bims-mitmed Biomed News
on Mitochondrial medicine
Issue of 2026–04–26
twenty-six papers selected by
Dario Brunetti, Fondazione IRCCS Istituto Neurologico



  1. Nat Commun. 2026 Apr 20. pii: 3570. [Epub ahead of print]17(1):
      Leigh syndrome (Leigh) is an untreatable mitochondrial disorder characterized by lactic acidosis and basal ganglia and midbrain pathology, leading to psychomotor regression and early death. We previously uncovered impaired neuronal morphogenesis in Leigh cerebral organoids carrying SURF1 gene variants. Leveraging this phenotype, we here develop a deep learning algorithm tailored for cell type-specific drug repurposing screening. In parallel, we perform a survival drug screen in a yeast model of Leigh. The two approaches independently converge on azole compounds, two of which - talarozole and sertaconazole - rescue neuronal morphogenesis in Leigh neurons and lower lactate release and improve growth rate in Leigh midbrain organoids. Mechanistically, these compounds modulate the retinoic acid pathway and membrane-associate lipid metabolism. The findings highlight azoles as promising candidates for Leigh and demonstrate the potential of combining in silico screens with human brain organoids as new approach methodologies (NAMs) to advance the discovery of therapeutics addressing rare neurodevelopmental disorders.
    DOI:  https://doi.org/10.1038/s41467-026-71391-2
  2. Clin Transl Sci. 2026 May;19(5): e70565
      Nomlabofusp is a recombinant, cell-penetrating human frataxin (hFXN) fusion protein in development for the treatment of Friedreich's ataxia (FRDA). This study evaluated whether nomlabofusp-derived hFXN concentrations covary across accessible peripheral matrices and FRDA-relevant tissues, supporting the feasibility of surrogate tissue sampling to monitor drug-derived hFXN exposure. Following subcutaneous administration in mice, rats, non-human primates, and patients with FRDA, we quantified nomlabofusp-derived hFXN and assessed cross-tissue correlations across target tissues (brain, heart, skeletal muscle, dorsal root ganglia) and accessible peripheral matrices (skin, buccal cells, platelets). We observed significant and consistent cross-tissue correlations, with concordant relationships among heart, skeletal muscle, dorsal root ganglia, skin, buccal cells, liver, and mitochondrial fractions, indicating coordinated distribution and/or retention of nomlabofusp-derived hFXN across these matrices. Correlation patterns were maintained across species, supporting the robustness and translational relevance of the observed relationships. Collectively, these data support the use of peripheral tissues-particularly skin and buccal cells-for cross-sectional and longitudinal monitoring of hFXN supplementation in FRDA.
    Keywords:  Friedreich's ataxia; cell‐penetrating peptide; frataxin; nomlabofusp; preclinical; surrogate tissue
    DOI:  https://doi.org/10.1111/cts.70565
  3. J Transl Med. 2026 Apr 24.
      
    Keywords:  Aging; Mitochondria; Mitochondrial biogenesis; Mitochondrial dysfunction; Mitophagy; NAD+; Oxidative stress; PGC-1α; Rejuvenation; Sirtuins
    DOI:  https://doi.org/10.1186/s12967-026-08047-8
  4. Redox Biol. 2026 Apr 14. pii: S2213-2317(26)00164-3. [Epub ahead of print]93 104166
      Mitochondria and peroxisomes communicate to maintain lipid homeostasis, but how the latter adjust to mitochondrial dysfunction remains unclear. Here, we show that loss of complex I subunit NDUFS4 in mouse fibroblasts leads to impaired mitochondrial fatty acid oxidation, resulting in the accumulation of triacylglycerol and lipid droplet (LD) expansion. In this context, peroxisomal biogenesis is upregulated, but their β-oxidation capacity is impaired, suggesting an adaptive yet ineffective response. Additionally, lipid overload using a very-long-chain fatty acid (VLCFA) leads to peroxisomal proliferation but prevents LD expansion when peroxisomal β-oxidation is compromised. The data demonstrated that proper peroxisomal processing is necessary for lipid storage under mitochondrial stress conditions. Our findings reveal a peroxisomal maladaptive remodelling response that fails to compensate for mitochondrial dysfunction, leading to disruptions in LD homeostasis. We propose a critical axis involving peroxisomes-LD-mitochondria that buffers metabolic stress in mitochondrial diseases.
    Keywords:  Complex I dysfunction; Lipid homeostasis; Mitochondria-peroxisome crosstalk; NDUFS4-KO; Peroxisomes
    DOI:  https://doi.org/10.1016/j.redox.2026.104166
  5. Front Neurol. 2026 ;17 1793054
      Leigh syndrome (LS) is a prevalent mitochondrial encephalomyopathy in childhood, triggered by mutations in mitochondrial DNA (mtDNA) or nuclear DNA (nDNA). The protein encoded by the SURF1 gene localizes to the inner mitochondrial membrane and is involved in the biosynthesis of the cytochrome c oxidase (COX) complex. We enrolled 5 children harboring SURF1 gene variants whose clinical manifestations were highly consistent with LS. The clinical characteristics and potential pathogenic mechanisms of the disease were elucidated by systematic analysis of their clinical data. Among the 5 patients, 4 were female and 1 was male, with ages ranging from 13 months to 2 years and 7 months. Next-generation sequencing (NGS) results revealed 6 variant sites in the SURF1 gene among the 5 patients, of which 2 were known variants and 4 were unreported novel variants, namely c.314-317delTGCC (p.L105Qfs*7), c.588+1_588+3delGTA (splicing), c.655G>T (p.Glu219), and c.515+3G>C. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed on the peripheral blood of 4 patients, and the results demonstrated that the messenger RNA (mRNA) expression level of the SURF1 gene was significantly lower than that in their parents. Using 10 healthy children as controls, we analyzed the ratios of mitochondria-related NADH-ubiquinone oxidoreductase core subunit 1 (ND1), Cytochrome c oxidase subunit I (COX1), Cytochrome c oxidase subunit II (COX2), NADH-ubiquinone oxidoreductase chain 4 (ND4), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as a nuclear reference gene. Mitochondrial DNA content was determined by measuring the ND1/GAPDH ratio using RT-qPCR, and further verified with COX1, COX2, and ND4. These ratios were all significantly decreased, indicating reduced mitochondrial DNA (mtDNA) copy number/mtDNA depletion. Iterative Threading ASSEmbly Refinement (I-TASSER)-based three-dimensional (3D) structural analysis indicated that all 6 variant sites induced alterations in the spatial structure of the SURF1 protein. The SURF1 protein is a hydrophilic protein, protein hydrophobicity and stability analyses showed that the 4 unreported novel variants could reduce the hydrophilicity, increase the hydrophobicity, and decrease the structural stability of the protein. The Saccharomyces cerevisiae Homolog of Yeast 1 (Shy1) domain serves as the key structural basis for SURF1 to exert its mitochondrial functions. We found that all 6 variant sites in the SURF1 gene were located within the Shy1 domain.
    Keywords:  Chinese children; Leigh syndrome; Shy1 domain; mitochondrial DNA depletion; splice-site variant
    DOI:  https://doi.org/10.3389/fneur.2026.1793054
  6. Eur J Hum Genet. 2026 Apr 21.
      Mitochondrial disorders (MDs) are a diverse group of genetic conditions primarily affecting the oxidative phosphorylation (OXPHOS) system and cellular energy production. Among MDs, Linear Skin Defects with Multiple Congenital Anomalies (LSDMCA), or Microphthalmia with Linear Skin Lesions (MLS) syndrome, is a rare X-linked dominant male-lethal disorder characterized by ocular malformations, linear skin defects, and multisystem developmental anomalies. These features are associated with pathogenic variants in genes related to mitochondrial function, including HCCS, COX7B, and NDUFB11 or chromosomal rearrangements of the Xp22 region encompassing HCCS. Despite progress, genotype-phenotype correlations remain insufficiently defined. In this study, we report three novel mutations in three patients with LSDMCA, broadening the phenotypic spectrum of the disorder. Whole exome sequencing revealed pathogenic missense variants in HCCS [NM_005333.5: c.625 G > C; p.(Asp209His)] and COX7B [NM_001866.3: c.221 C > T; p.(Pro74Leu)] in two unrelated patients. Functional studies confirmed that the COX7B variant impairs mitochondrial respiratory chain (MRC) function. A third patient harbored a novel frameshift pathogenic variant in NDUFB11 [NM_001135998.3: c.145_152dup; p.(Thr52Glnfs*66)], further implicating mitochondrial dysfunction in LSDMCA pathogenesis. Notably, the COX7B variant was identified in a biological male (46, XY) without X-chromosome structural rearrangements, marking the first such reported case of LSDMCA. Our data suggest that certain missense variants, resulting in mild impairment of the gene product, may allow male survival, thereby expanding the known phenotype of this rare disorder. This report advances our understanding of genotype-phenotype correlations in LSDMCA and highlights the impact of mitochondrial dysfunction during embryonic development.
    DOI:  https://doi.org/10.1038/s41431-026-02098-7
  7. Autophagy. 2026 Apr 23. 1-15
      HSAN9 is a rare progressive neurodegenerative disease in children linked to bi-allelic loss-of-function mutations in the TECPR2 gene. TECPR2 is a multi-domain protein harboring N-terminal WD repeats and C-terminal TECPR repeats, followed by a functional LIR motif that serves in phagophore targeting. Here, we demonstrate that the absence of TECPR2 results in impaired mitophagy, which can be restored by expressing its C-terminal domain. Accordingly, we uncover severe mitochondrial dysfunction and accumulation of mitochondrial content in primary fibroblasts derived from an HSAN9 patient, as well as in embryonic fibroblasts and dorsal root ganglia derived from an HSAN9 mouse model. Notably, these mitochondrial defects are mediated by mitochondrial stress through the activation of the integrated stress response (ISR), whereas mitochondrial function is restored by pharmaceutical or genetic suppression of ISR. Our findings establish a new connection between mitophagy and ISR in maintaining mitochondrial homeostasis during neurodegeneration.Abbreviations: Baf. A1: bafilomycin A1; CYCS: cytochrome c, somatic; HSAN9: hereditary sensory and autonomic neuropathy IX; ISR: integrated stress response; OA: oligomycin + antimycin A; ROS: reactive oxygen species; TECPR2: tectonin beta-propeller repeat containing 2.
    Keywords:  HSAN9; TECPR2; integrated stress response; mitophagy; neurodegeneration; unfolded protein response
    DOI:  https://doi.org/10.1080/15548627.2026.2660850
  8. Nat Commun. 2026 Apr 18. pii: 3589. [Epub ahead of print]17(1):
      Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life. While genetic distortions of mitochondrial integrity elicit premature aging, the mechanisms leading to "natural" aging of mitochondria are less clear. Here we use proteomics, lipidomics, genetics and functional tests in wild type Caenorhabditis elegans and long-lived clk-1(qm30) and isp-1(qm150) mitochondrial mutants to identify molecular pathways that support longevity amid persistent mitochondrial inefficiency. These tests and subsequent transcriptomics and metabolomics analyses in humans reveal aging-associated decline of phosphatidylcholine synthesis as a trigger of mitochondrial network disruption, which contributes to mitochondrial dysfunction during normal aging. Moreover, ectopic boosting of phosphatidylcholine levels via diet restores late life mitochondrial integrity in vivo in nematodes and reinstates metabolic resilience in human cell culture tests. We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
    DOI:  https://doi.org/10.1038/s41467-026-71508-7
  9. iScience. 2026 May 15. 29(5): 115530
      Localized protein translation enables spatially restricted cellular dynamics, particularly in neurons, where specific mRNAs are translated in axons and dendrites far from the cell body. Translating ribosome affinity purification (TRAP) has been used to study axonal translation in rodents and cell-type-specific translation in Drosophila, but existing protocols are not optimized for axons, where material is extremely limited. Here, we present a highly sensitive TRAP protocol for isolating ribosome-bound mRNAs from low-input samples, enabling recovery of axonal mRNAs from Drosophila larval and adult (leg) motor neurons. RNA-seq identified axonally translated transcripts, including mRNAs encoding ribosomal and mitochondrial proteins, similar to those reported in axons of other species, indicating conservation of axonal translation in Drosophila. This low-input method enables analysis of local translation with Drosophila genetics across developmental stages, genetic backgrounds, and disease models, and can be adapted for rare genotypes, other tissues and model systems requiring high sensitivity.
    Keywords:  genetics; molecular biology; neuroscience
    DOI:  https://doi.org/10.1016/j.isci.2026.115530
  10. Autophagy. 2026 Apr 23.
      Mitochondrial quality control is essential for maintaining neuronal function and resilience during aging, yet pharmacological strategies that effectively restore mitophagy to maintain mitochondrial homeostasis remain limited. Emerging evidence suggests that dietary molecules may influence mitochondrial health, although the underlying mechanisms are largely unknown. Here, we summarize our recent finding whereby we have identified a robust mitophagy inducer: α-amyrin (αA). This molecule is a lipid-like pentacyclic triterpenoid abundant in edible plants, such as passion fruit. Mechanistically, αA targets dual leucine zipper kinase (DLK), a neuron-enriched stress kinase that plays a central role in axonal degeneration signaling. Under pathological stress, DLK activates the degeneration mediator SARM1, which can sequester the key autophagy/mitophagy protein ULK1 leading to compromised autophagy and mitophagy. By specifically binding to DLK, αA releases ULK1 from SARM1-mediated restriction and promotes ULK1-dependent mitophagy, restoring mitochondrial homeostasis. This mechanism reveals the DLK-SARM1-ULK1 cascade as a previously underappreciated regulatory interface linking neuronal stress signaling to mitochondrial surveillance pathways. More broadly, these findings introduce lipid-like dietary molecules as potential "mitochondrial guardians" that preserve organelle integrity through physiological activation of mitophagy. Targeting the DLK-SARM1-ULK1 axis with such molecules may represent a promising strategy for maintaining mitochondrial health and mitigating neurodegenerative processes associated with aging.
    Keywords:  DLK; ULK1; lipid-like molecule; mitophagy; α-amyrin
    DOI:  https://doi.org/10.1080/15548627.2026.2664599
  11. Mol Neurobiol. 2026 Apr 22. pii: 580. [Epub ahead of print]63(1):
      Friedreich's Ataxia (FRDA) is an early onset hereditary disorder with a strong neurodegenerative component caused by repeat expansions on the gene encoding for frataxin (FXN) that result in FXN deficiency. This deficit has been linked to a cascade of biochemical alterations, including mitochondrial dysfunction, oxidative stress and neuronal apoptosis, that drives the neurodegenerative process. FRDA is a very incapacitating disease and patients rely on very limited therapeutic alternatives, such as the recently approved drug omaveloxolone, to treat the oxidative stress. Nevertheless, previous studies have suggested the activation of the brain-derived neurotrophic factor (BDNF) may be a promising treatment to regulate FRDA pathophysiology. Herein, we characterize the effects of FXN deficiency in an in vitro model of primary cerebellar granule neurons (CGNs) derived from the FRDA mouse model YG8-800, as well as the therapeutic potential of BDNF partial agonism by the small molecule 7,8-dihydroxyflavone (7,8-DHF). We found evidence of mitochondrial dysfunction concomitant with DNA damage and enhanced cell death due to FXN deficiency in cultured neurons. The treatment with 7,8-DHF was able to reduce the markers of genotoxicity and apoptosis, without restoring the impaired mitochondrial function nor the total cell death, possibly through ferroptosis, revealing a partial neuroprotective effect insufficient to halt the neurodegenerative process in this in vitro model of FRDA.
    Keywords:  7,8-dihydroxyflavone; Apoptosis; DNA damage; Ferroptosis; Friedreich’s ataxia; Neurodegeneration
    DOI:  https://doi.org/10.1007/s12035-026-05856-2
  12. Environ Health. 2026 Apr 22.
      
    Keywords:  Birth weight; Environmental pollutants; Fetal development; Polychlorinated biphenyls; Prenatal exposure
    DOI:  https://doi.org/10.1186/s12940-026-01263-1
  13. Am J Med. 2026 Apr 17. pii: S0002-9343(26)00288-3. [Epub ahead of print]
      The principal cellular energy-generating pathways of mitochondria used to produce adenosine triphosphate (ATP) are oxidative phosphorylation and β-oxidation of fatty acids. Under anaerobic conditions, glycolysis in the cytoplasm is an alternative mechanism for production of ATP. Mitochondrial diseases result from one or more of the over 350 mutations in mitochondrial DNA (10%) or nuclear DNA (90%) that cause defective mitochondrial ATP production. The most common manifestations in adults with mitochondrial DNA mutations are diminished vision, myopathy, cardiomyopathy, neuropathy, encephalopathy and diabetes. Uncommonly there are stroke-like syndromes. The most common manifestations in adults with nuclear DNA mutations are neuropathy with prominent ataxia, ophthalmoplegia, dysarthria, myopathy, cardiomyopathy, liver disease, neuroendocrine and renal cell tumors, and hypoglycemia. Adults, especially the elderly, may only develop manifestations in the course of stressful illnesses that unmask these mutations. Children may require mitochondrial transfer or gene editing therapy. These mutations should be sought in leukocytes or muscle tissue in adults who do not respond to usual treatment for severe stressful illnesses as they may benefit from newly-approved medications.
    Keywords:  Oxidative phosphorylation; anaerobic glycolysis; fatty acid β-oxidation; gene editing; mitochondrial transfer; reactive oxygen species (ROS)
    DOI:  https://doi.org/10.1016/j.amjmed.2026.04.018
  14. Sci Adv. 2026 Apr 24. 12(17): eaed6824
      Enterovirus D68 (EV-D68) is a plus-strand RNA virus that primarily causes respiratory infections in infants but, in rare cases, has been associated with the pediatric paralytic disease acute flaccid myelitis. We previously demonstrated that EV-D68 induces nonselective autophagy for its benefit. Here, we demonstrate that the 3C protease of EV-D68 cleaves the mitochondrial fusion protein Mitofusin 2 near its C-terminal HR2 domain, inducing fragmentation of the mitochondrial network. This, in turn, triggers the formation of mitophagosomes, a hallmark of mitophagy, a selective form of autophagy that recycles mitochondria. Multiple hallmarks of mitophagy are observed during infection, including loss of mitochondrial membrane potential and Parkin translocation to the mitochondria, but mitochondrial degradation is blocked during infection. While autophagy plays multiple roles in enterovirus infection, depleting Mitofusin 2 or transiently overexpressing Mitofusin 2, particularly the cleavage-resistant mutant, specifically reduces EV-D68 release from cells without affecting intracellular titers. Our results show that enteroviruses induce mitophagosomes as vectors for nonlytic release of virions from cells.
    DOI:  https://doi.org/10.1126/sciadv.aed6824
  15. Protein Sci. 2026 May;35(5): e70553
      Mitochondria are essential organelles that drive numerous cellular processes, including energy metabolism, ion homeostasis, and programmed cell death. This functional versatility relies on a highly dynamic proteome whose composition is continuously remodeled to meet changing cellular and environmental demands. Central to this remodeling are mitochondrial proteases (termed mitoproteases), which maintain protein quality and regulate mitochondrial function through selective processing and degradation events. Their activity ensures rapid degradation of regulatory proteins and dynamically adjusts components of multiprotein complexes. Among their most critical targets are elements of the mitochondrial protein import machinery. By modulating translocase stability and by processing preproteins during translocation, mitoproteases enable precise control over the organelle's proteome, aligning mitochondrial function with the cell's metabolic state. This review discusses how mitoproteases maintain translocase integrity and dynamically regulate mitochondrial protein import and the mitochondrial proteome.
    Keywords:  mitochondrial proteases; mitochondrial protein import; mitochondrial remodeling; protein quality control
    DOI:  https://doi.org/10.1002/pro.70553
  16. Trends Endocrinol Metab. 2026 Apr 22. pii: S1043-2760(26)00045-7. [Epub ahead of print]
      Evolved constraints to human energy transformation force the body-brain system to operate an economy of energy. To survive and thrive, an organism's finite internal energy resources must be dynamically reallocated, forcing trade-offs from organelle to organism. Building on an energy trade-off framework integrating life history theory and cellular biology, we propose that energy trade-offs occur between three main classes of processes relevant to health: (i) vital, (ii) stress, and (iii) growth, maintenance, and repair (GMR). Competing demands for these processes exist within a hierarchy of energy needs where more 'urgent' vital- and stress-related functions are prioritized by suppressing longevity-promoting growth, maintenance, and repair processes. The energy constraint model of human health provides an energy-based framework to address health/disease dynamics across the lifespan.
    Keywords:  aging; bioenergetics; disease; energy compensation; evolution; exercise; healing; metabolic compensation; mind-body; mitochondria; stress; trade-offs
    DOI:  https://doi.org/10.1016/j.tem.2026.02.010
  17. Sci Immunol. 2026 Apr 24. 11(118): eaed2623
      Animals engage pleiotropic immune defense mechanisms to survive infections. Here, we present a function for mitochondrial fission in host defense. Challenge of macrophages with Escherichia coli increased mitochondrial fission, with this response promoting bacterial clearance in mammalian macrophages and Caenorhabditis elegans. E. coli-induced mitochondrial fission engaged dual antibacterial responses via the mitochondrial unfolded protein response (UPRmt) and inducible lipid droplet production. Mitochondrial fission-triggered UPRmt, characterized by activation of activating transcription factor 5 (ATF5) in mouse macrophages and the paralog ATFS-1 in C. elegans, curtailed inducible lipid droplets to cross-regulate these pathways. The intramacrophage pathogen Salmonella enterica suppressed antibacterial mitochondrial fission, but restoring this response by inhibiting mitochondrial fusion-promoting histone deacetylase 6 (HDAC6) reactivated lipid droplet production and bacterial clearance. Therefore, we propose that mitochondrial fission is an ancient host defense pathway that can be exploited for anti-infective design.
    DOI:  https://doi.org/10.1126/sciimmunol.aed2623
  18. Nat Commun. 2026 Apr 21.
      The mitochondrial respiratory chain (MRC) complexes, crucial for aerobic energy transduction in eukaryotes, form conserved higher-order structures called supercomplexes (SCs). The elucidation of SC physiological relevance is critical for our understanding of mitochondrial function and bioenergetics but has been hindered by the limited availability of experimental models isolating SC formation as the sole variable. In baker's yeast, SCs comprise III2IV1 and III2IV2 configurations, which enhance respiratory rates by facilitating cytochrome c diffusion along the SC surface. However, the roles of distinct SC conformations and MRC plasticity remain unclear. To address these questions, we engineered a yeast strain expressing a covalently-linked III2IV2 SC, structurally like the wild-type. Expression of this tethered SC supports robust respiratory activity but selectively impacts cytosolic NADH-driven respiration, due to distinct interactions with the NADH dehydrogenase Nde1. We propose that in yeast mitochondria, substrate-specific respirasome-like SCs contribute to the optimization of electron fluxes and support metabolic flexibility.
    DOI:  https://doi.org/10.1038/s41467-026-72228-8
  19. Chem Biol Interact. 2026 Apr 22. pii: S0009-2797(26)00197-3. [Epub ahead of print] 112089
      Sepsis-associated acute kidney injury (SA-AKI) is closely linked to profound metabolic reprogramming and mitochondrial dysfunction, yet effective metabolic targeted therapies remain limited. In this study, we elucidated the molecular mechanism by which ethyl pyruvate (EP), an exogenous metabolic substrate, alleviates SA-AKI by regulating mitochondrial bioenergetics through the AMPK-mTOR-SIRT3 signaling pathway. Using a cecal ligation and puncture-induced SA-AKI mouse model and LPS-stimulated HK-2 cells, we demonstrated that EP synergized with the AMPK activator AICAR to significantly improve renal function, reduce injury markers and inflammation, and enhance survival. Single-cell RNA sequencing (scRNA-seq) identified extensive metabolic reprogramming in renal epithelial cells during sepsis, characterized by mitochondrial dysfunction and suppression of oxidative phosphorylation (OXPHOS). Mechanistically, combined EP and AICAR treatment, rather than EP alone, alleviated mitochondrial dysfunction by restoring NAD+/NADH balance, increasing mitochondrial DNA (mtDNA) content, improving mitochondrial respiratory chain complex activity, and rebalancing mitochondrial fission-fusion dynamics. Combined EP and AICAR treatment also enhanced autophagy and reduced apoptosis, partly through a SIRT3-dependent mechanism downstream of AMPK-mTOR signaling. This effect was enhanced or diminished by pretreatment with rapamycin (Rapa) or interferon-γ (IFN-γ). Pharmacological inhibition of SIRT3 partially abolished the mitochondrial and cytoprotective benefits of EP, confirming SIRT3 as a key downstream effector of AMPK-mTOR signaling. Collectively, our data identified EP as a metabolic modulator that synergizes with AMPK activation to alleviate SA-AKI. This effect is achieved by restoring mitochondrial function and OXPHOS through the AMPK-mTOR-SIRT3 signaling pathway, providing a mechanistic basis for metabolism-oriented therapeutic strategies in SA-AKI.
    Keywords:  AMPK; Ethyl pyruvate (EP); Metabolic reprogramming; Mitochondrial bioenergetics; SIRT3; Sepsis-associated acute kidney injury (SA-AKI)
    DOI:  https://doi.org/10.1016/j.cbi.2026.112089
  20. Lancet Neurol. 2026 May;pii: S1474-4422(26)00082-7. [Epub ahead of print]25(5): 469-481
       BACKGROUND: Friedreich's ataxia is a rare, chronic, progressive, neurodegenerative condition affecting multiple organ systems, including neurological, musculoskeletal, cardiac, and endocrine systems, and is marked by low cardiopulmonary fitness. We tested the effect of exercise and NAD+ precursor supplementation with nicotinamide riboside, which have each shown benefits in animal and early clinical studies, on cardiopulmonary fitness in individuals with Friedreich's ataxia.
    METHODS: This 12-week, outpatient, phase 2, single-site (Children's Hospital of Philadelphia, Philadelphia, PA, USA), randomised, 2 × 2 factorial clinical trial recruited individuals aged 10-40 years with an ejection fraction of 45% or greater who were able to exercise. A computer-generated randomisation sequence was developed by the trial statistician. Random allocation was age-stratified (<18 years vs ≥18 years) to one of four groups: placebo and no exercise with attention control (weekly phone calls; henceforth placebo only), nicotinamide riboside and no exercise with attention control (henceforth nicotinamide riboside only), placebo and exercise (exercise only), and nicotinamide riboside and exercise (combination therapy). Individualised exercise plans were developed by the exercise physiologist (three aerobic and two resistance training sessions weekly), performed at the individual's home, and overseen remotely (telephone check-ins by the physiologist). Weight-based dosing of nicotinamide riboside or placebo was 300 mg (1 capsule) for weights of 24 kg up to 48 kg, 600 mg (2 capsules) for weight 48 kg up to 72 kg, and 900 mg (3 capsules) for weights of over 72 kg. The primary outcome was change in peak VO2 (L/min) during cardiopulmonary exercise testing at 12 weeks versus baseline, and the effect of treatment group was assessed in a statistical model accounting for age (stratification variable), sex, and baseline peak VO2. Stage 1 analysis tested the difference between each active treatment versus the control group, and stage 2 analysis (if combination therapy was effective) tested the difference between combination treatment and exercise alone; family-wise type 1 error was maintained <0·05. Analyses were by intention-to-treat. Adverse events were recorded systematically. This trial is registered with ClinicalTrials.gov (NCT04192136) and is complete.
    FINDINGS: Between Sept 3, 2020, and April 23, 2025, we enrolled 74 individuals, of whom 66 met the eligibility criteria and were randomly allocated to the four study groups. All participants completed the study. 33 (50%) were children (aged 10-17 years) and 33 (50%) were adults (aged ≥18 years); 37 (56%) were male and 29 (44%) were female. Least mean squares for the change in peak VO2 in L/min were -0·05 (95% CI -0·16 to 0·06) for the 17 participants in the control group; 0·06 (-0·05 to 0·17) for the 17 participants in the nicotinamide riboside and no exercise group; 0·11 (0·00 to 0·22) for the 16 participants in the placebo and exercise group; and 0·16 (0·05 to 0·27) for the 16 participants in the nicotinamide riboside and exercise group. Differences between active treatment and the control group were 0·10 (95% CI -0·05 to 0·26; padjusted=0·188) for nicotinamide riboside and no exercise; 0·16 (0·00 to 0·31; padjusted=0·103) for placebo and exercise; and 0·21 (0·05 to 0·36; padjusted=0·0299) for nicotinamide riboside and exercise in combination. Combination therapy was not statistically different from exercise alone (difference -0·05 ([95% CI -0·10 to 0·21]; p=0·49). Adverse events were all mild or moderate, and included gastrointestinal symptoms, falls, upper respiratory infections, and skin rashes. At least one moderate adverse event of interest in these categories was reported by seven (41%) participants in the control group; six (35%) in the nicotinamide riboside and no exercise group; three (19%) in the placebo and exercise group; and four (25%) in the nicotinamide plus exercise group.
    INTERPRETATION: The combination of nicotinamide riboside plus exercise for 12 weeks was safe and increased cardiopulmonary fitness in children and adults with Friedreich's ataxia. Longer studies are needed to establish whether adding nicotinamide riboside to exercise could be considered as part of a long-term, comprehensive treatment approach.
    FUNDING: US National Institutes of Health and Friedreich's Ataxia Research Alliance.
    DOI:  https://doi.org/10.1016/S1474-4422(26)00082-7
  21. J Biol Chem. 2026 Apr 17. pii: S0021-9258(26)00347-9. [Epub ahead of print] 111475
      Mitochondrial disease can result from mutations in the enzymes responsible for biosynthesis of heme a and hemylation of respiratory complex IV of the electron transport chain, also known as cytochrome c oxidase (CcO). One of these enzymes, which is essential for assembly and function of CcO and thus function of the electron transport chain, is heme a synthase, COX15. A previously unknown fatal missense mutation of COX15, c.232G>A (p.Gly78Arg), was recently described in a case report by Galvão de Oliveira et al. Here, we show that the p.Gly78Arg-mimicking substitution in the homologous Cox15 protein in Saccharomyces cerevisiae (Gly95Arg) causes Cox15 protein instability and recapitulates the CcO defect observed in the patient. We demonstrate that the CcO defect observed with this Cox15 variant stems from insufficient heme a synthesis, and consequently, insufficient CcO hemylation and decreased levels of CcO. Our results provide insights into the etiology of the disease caused by this variant, suggesting that Cox15 protein instability and consequent attenuation of heme a synthase function is the main molecular factor behind the resulting multisystemic mitochondrial disorder in humans.
    Keywords:  COX15; Cytochrome c oxidase; Heme; Heme A Synthase; Mitochondria; Yeast model
    DOI:  https://doi.org/10.1016/j.jbc.2026.111475
  22. FEBS Lett. 2026 Apr 24.
      The placenta plays a vital role in supporting and nourishing the fetus throughout pregnancy, yet the mechanisms governing its development remain poorly understood. Recent advances in 3D human trophoblast organoid systems derived from both primary tissues and stem cells provide physiologically relevant platforms to investigate placental development in both health and disease. This 'In a Nutshell' review highlights how these models are transforming our ability to investigate human placental biology in pregnancy.
    Keywords:  development; maternal–fetal interactions; organoids; placenta; pregnancy; reproduction; trophoblast
    DOI:  https://doi.org/10.1002/1873-3468.70344
  23. Genes Dev. 2026 Apr 22.
      During cortical development, neural stem cells (NSCs) combine self-renewal with the sequential production of different subtypes of projection neurons as well as glia cells. How the NSC epigenome accommodates this over time remains unresolved. Here, we address this gap by multimodal epigenomic profiling of mouse cortical development across six time points and five embryonic days. Single-cell gene expression and temporal modeling reveal that NSC self-renewal is not homeostatic, showing progressively stronger astrocytic preference over time. Chromosome accessibility, DNA methylation, and Hi-C show that this process involves major reorganization of the NSC epigenome. A model combining transcription factor motif affinities with epigenetic features, as well as integration of the results with a reporter assay in vivo, show that activation of the NSC neuronal fate regulatory program may be affected by a changing epigenome. Collectively, our findings uncover temporal epigenomic reprogramming that underlies the evolving differentiation potential of NSCs, providing insights into the intrinsic and extrinsic mechanisms that pattern cortical lineages.
    Keywords:  brain development; computational modeling; epigenetics; in vivo MPRA; single-cell omics
    DOI:  https://doi.org/10.1101/gad.353090.125
  24. Nat Commun. 2026 Apr 22.
      Mitochondrial dysfunction is a major contributor to myocardial ischemia-reperfusion injury, and limits cardiac recovery after blood flow is restored. Although mitochondria transplantation may help restore cellular energy metabolism, its therapeutic benefit is reduced by extracellular calcium-induced mitochondrial damage. Here we show that a thermosensitive phase-separated hydrogel made of gelatin and PEG can condense, protect and deliver freshly isolated mitochondria. Compared with conventional single-phase hydrogels, this system remains injectable at physiological temperature and enables rapid mitochondria release after transplantation. Furthermore, the phase-separated structure improves mitochondrial packing and preserves activity through spatial confinement and calcium chelation by gelatin. In vitro, condensed mitochondria show improved membrane potential and ATP production. In vivo, transplanted mitochondria are efficiently internalized by cardiomyocytes, improving cardiac function and reducing tissue injury after myocardial ischemia-reperfusion. These findings identify phase-separated hydrogels as a promising platform for mitochondria transplantation.
    DOI:  https://doi.org/10.1038/s41467-026-71765-6