bims-ripira Biomed News
on RRM2B MDMD in Adults
Issue of 2026–04–12
fifteen papers selected by
Martín Lopo
  1. Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.
  2. Non-invasive biomarkers for diagnosis and monitoring of primary mitochondrial diseases.
  3. Ophthalmic manifestations of mitochondrial disorders.
  4. Associations of Elevated Red Cell Distribution Width (RDW) with Decreased Physical and Cognitive Function in Older Adults, and The Potential Mediation by Mitochondrial Energetics: The Study of Muscle, Mobility and Aging (SOMMA).
  5. Low-intensity pulsed ultrasound restores mitochondrial dynamics and function in lipopolysaccharide-stimulated astrocytes.
  6. ADT-OH promotes mitophagy and suppresses the cytosolic mtDNA-cGAS-STING inflammatory cascade in microglia.
  7. Rethinking Mitochondria: The Extracellular Dimension.
  8. A unified ACSF3-mtFAS model linking mitochondrial energy metabolism to human anthropometric evolution.
  9. Paroxysmal movement disorders: an update on genetics, mechanisms, and emerging therapeutic strategies.
  10. Biomarkers in predicting mortality among ICU patients with sepsis.
  11. Periosteal mitochondria DNA structures drive aging-associated poor skeletal repair.
  12. Mitochondrial dysfunction in Alzheimer's disease and related sex differences.
  13. Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.
  14. Mitochondrial Transfer: From Bench to Bedside.
  15. Moxibustion delays ovarian aging by regulating mitochondrial biogenesis and improving oocyte quality.
  1. Circ Res. 2026 Apr 10. 138(8): e326985
    Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.
    Xi Fang, Åsa B Gustafsson.
      Mitochondria are highly dynamic, double-membraned organelles that generate the majority of ATP in cardiomyocytes while supporting cellular homeostasis and signal transduction. Accumulation of dysfunctional mitochondria can promote cardiomyocyte loss, impair contractile function, and ultimately lead to myocardial damage. To preserve mitochondrial integrity, cardiomyocytes rely on multilayered quality control mechanisms to remove defective mitochondria. Two major routes have emerged for this process: degradation, primarily via autophagy, and secretion via extracellular vesicles. This review summarizes the mechanisms of mitochondrial degradation and secretion in the heart and highlights their contributions to cardiac disease progression and potential as therapeutic targets.
    Keywords:  extracellular vesicles; homeostasis; mitochondria; mitophagy; myocytes, cardiac
    DOI:  https://doi.org/10.1161/CIRCRESAHA.125.326985
  2. J Neurol. 2026 Apr 10. pii: 263. [Epub ahead of print]273(5):
    Non-invasive biomarkers for diagnosis and monitoring of primary mitochondrial diseases.
    Ignazio Giuseppe Arena, Shamini Saravanabavan, Rita Horvath, Jelle van den Ameele.
      Primary mitochondrial diseases (PMDs) represent a clinically and genetically heterogeneous group of disorders characterized by impaired oxidative phosphorylation and multisystem involvement, commonly affecting the nervous system. As therapeutic development accelerates, there is a growing need for robust biomarkers capable of supporting diagnosis, stratifying patient subgroups, monitoring disease progression, and providing sensitive pharmacodynamic readouts for clinical trials. This review summarizes recent advances in three major non-invasive biomarker domains relevant to PMDs: circulating serum and molecular biomarkers, functional and digital endpoints, and neuroimaging modalities. Circulating markers, such as FGF21, GDF15, NfL, and NAD⁺-related signatures, have each been proposed for diagnosis and to follow disease progression, while multi-omics approaches are paving the way toward integrated molecular phenotyping. Digital health technologies, including accelerometry and gait analytics, enable objective quantification of real-world functional impairment, although disease-specific validation remains an unmet need. Neuroimaging offers mechanistic insights through metabolic (MRS, CEST), perfusion (ASL), and molecular modalities (mitochondrial PET tracers). Cutting-edge tools, such as Multi-Spectral Optoacoustic Tomography (MSOT), Raman spectroscopy, and Near-Infrared Spectroscopy (NIRS), promise real-time or spatially resolved assessment of mitochondrial function. Together, these developments outline multidimensional biomarker approaches for PMDs, with the potential to directly measure target engagement and clinically meaningful phenotypes in future therapeutic trials. Future progress will depend on longitudinal validation, harmonized acquisition protocols, and the integration of multimodal platforms to support upcoming therapeutic trials and precision medicine strategies.
    Keywords:  Biomarkers; Clinical trials; Digital health technologies; Functional endpoints; Magnetic resonance imaging; Mitochondrial disease; Neuroimaging; Phenotyping; Positron emission tomography; Precision medicine; Wearable devices
    DOI:  https://doi.org/10.1007/s00415-026-13794-1
  3. Prog Retin Eye Res. 2026 Apr 03. pii: S1350-9462(26)00032-7. [Epub ahead of print] 101466
    Ophthalmic manifestations of mitochondrial disorders.
    Megan F Baxter, Grace A Borchert, Emma L Blakely, Claire W Ruan, Robert E MacLaren, Robert McFarland, Robert W Taylor.
      Mitochondrial diseases are the most common group of inherited neurometabolic disorders and frequently involve multiple organ systems with high energy demands. Ophthalmic manifestations are a common occurrence in affected individuals and may be the earliest or predominant clinical feature. However, the marked clinical heterogeneity of mitochondrial eye disease often delays recognition and therefore diagnosis. Mitochondria play a central role in cellular metabolism through the process of oxidative phosphorylation. Genetic mutations in either nuclear DNA (nDNA) or mitochondrial DNA (mtDNA) can impair this key metabolic process leading to clinical disease. Diagnosing such mitochondrial diseases is however often complicated - the same genetic change can result in different symptoms (variable expressivity); different genes can cause similar conditions (allelic and locus heterogeneity); a single genetic change may affect multiple body systems (pleiotropy); and the proportion of affected mitochondrial DNA molecules can vary between tissues (mtDNA heteroplasmy). While the diagnostic process will certainly be influenced by the initial clinical presentation, perhaps more important is clinician awareness and early consideration of an underlying mitochondrial disorder. Early and accurate molecular genetic diagnosis is both available and essential, not only for prognostication and management, but also for reproductive counselling, access to appropriate clinical trials, cascade testing of relevant family members and consideration of emerging mitochondrial therapeutics(1,2). In this review, we summarise the biochemical and genetic foundations of mitochondrial eye disease, describe the spectrum of clinical phenotypes, outline diagnostic approaches and considerations, and highlight the importance of precise early diagnosis in guiding management and reproductive decision-making.
    Keywords:  mitochondria; mitochondrial counselling; ophthalmology
    DOI:  https://doi.org/10.1016/j.preteyeres.2026.101466
  4. Aging Dis. 2025 Apr 22. 17(3): 1654-1663
    Associations of Elevated Red Cell Distribution Width (RDW) with Decreased Physical and Cognitive Function in Older Adults, and The Potential Mediation by Mitochondrial Energetics: The Study of Muscle, Mobility and Aging (SOMMA).
    Kyoung Min Kim, Li-Yung Lui, Theresa Mau, Paul M Coen, Steven R Cummings.
      We analyzed the association between RDW and skeletal muscle mitochondrial energetics and how skeletal muscle mitochondrial energetics may mediate the associations of RDW with physical and cognitive performance. The study analyzed cross-sectional baseline data from the Study of Muscle, Mobility and Aging (SOMMA) that enrolled 864 participants aged 70 and older (mean=76.3 years). RDW, clinical and demographic parameters were assessed. Comprehensive evaluations were conducted for both physical and cognitive function using objective and subjective measures. Elevated RDW values were significantly correlated with decreased physical performance, evidenced by reduced cardiorespiratory fitness (VO2peak) and longer time to 400 m Walk, alongside impaired cognitive performance. Higher RDW values also demonstrated robust negative associations with various measurements of mitochondrial energetics, including maximal ATP production and oxidative phosphorylation. Mediation analysis revealed that impaired mitochondrial function partly mediated the associations between RDW values and VO2peak, and other physical and cognitive performance. These findings suggest that higher RDW is associated with declines in various physical and cognitive performance, with skeletal muscle mitochondrial energetics serving as a potential mediating factor. Causal inferences about potential mediation are limited by the cross-sectional design of the study. Nevertheless, the findings highlight the value of RDW as a potential biomarker for age-related declines in physical and cognitive function partly mediated by mitochondrial energetics.
    DOI:  https://doi.org/10.14336/AD.2024.1724
  5. Ups J Med Sci. 2026 ;131
    Low-intensity pulsed ultrasound restores mitochondrial dynamics and function in lipopolysaccharide-stimulated astrocytes.
    Umut Kerem Kolac, Aysegul Turkkol, Mahmut Alp Kılıc, Gizem Donmez Yalcın, Abdullah Yalcın, Mehmet Dincer Bılgın.
       Background: Low-intensity pulsed ultrasound (LIPUS) is a non-invasive therapeutic modality with growing potential in the treatment of neurodegenerative diseases. However, its mechanistic role in regulating mitochondrial homeostasis in astrocytes under inflammatory stress remains poorly understood. This study aimed to investigate the effects of LIPUS on mitochondrial dynamics, morphology, oxidative stress, mitochondrial membrane potential, and mitochondrial stress response in an in vitro model of neuroinflammation.
    Methods: Normal Human Astrocytes (NHA) were stimulated with lipopolysaccharide (LPS; 0.5 µg/mL, 24 h) and subsequently treated with LIPUS (1 MHz, 50% duty cycle, 100 Hz, 15 min) at intensities of 100, 300, or 500 mW/cm2. The expression of mitochondrial fusion (MFN1, MFN2, OPA1) and fission (DRP1, FIS1) markers was analyzed using qPCR. Mitochondrial morphology was evaluated by confocal microscopy, while reactive oxygen species (ROS) levels and mitochondrial membrane potential (ΔΨm) were measured using specific fluorescent probes. Expression of mitochondrial stress-related genes (PGC1α, CLPP, HSP60, LONP1) was also assessed.
    Results: LIPUS treatment, particularly at 300 mW/cm2, significantly enhanced the expression of mitochondrial fusion markers while suppressing fission markers in a dose- and time-dependent manner, with peak effects observed 4 h post-treatment. Confocal imaging revealed that LIPUS mitigated LPS-induced mitochondrial fragmentation. Additionally, LIPUS reduced ROS accumulation, preserved ΔΨm, and attenuated the LPS-induced upregulation of mitochondrial stress-related genes, suggesting modulation of both stress response and biogenesis.
    Conclusion: LIPUS ameliorates mitochondrial dysfunction in inflamed astrocytes by restoring mitochondrial dynamics and reducing stress signaling, supporting its potential as a therapeutic strategy for neuroinflammation-associated neurodegenerative disorders.
    Keywords:  LIPUS; astrocyte; lipopolysaccharide; mitochondrial dynamics
    DOI:  https://doi.org/10.48101/ujms.v131.13678
  6. Acta Pharmacol Sin. 2026 Apr 09.
    ADT-OH promotes mitophagy and suppresses the cytosolic mtDNA-cGAS-STING inflammatory cascade in microglia.
    Xiao-Ou Hou, Miao Wang, Rong Deng, Yi-Fan Lu, Jin-Ru Zhang, Li Ren, Jing Chen, Chun-Feng Liu, Ya-Ping Yang, Li-Fang Hu.
      Mitochondrial dysfunction, driven by genetic susceptibility or environmental insults, contributes to the pathogenesis of neurodegenerative disorders, including Parkinson's disease (PD). Mitophagy is a selective pathway that eliminates dysfunctional mitochondria, and mitophagy inducers hold therapeutic promise for neurodegeneration. However, the arsenal of specific, clinically viable inducers remains limited. ADT-OH, a slow-release H2S compound, was recently reported to induce mitochondrial uncoupling through sulfide-quinone oxidoreductase (SQR)-mediated oxidation of H2S. In this study, we report that ADT-OH elicits mitophagic flux in microglia. This is evidenced by the reduced steady-state levels of mitochondrial marker proteins (TOM20, COXIV, and HSP60), enhanced mitochondrial fission dynamics, and mitochondrial translocation into lysosomes, as visualized by the mt-Keima probe. Mechanistically, its mitophagy-promoting effect is dependent on SQR-mediated mitochondrial uncoupling and subsequent activation of PINK1-PARKIN signaling. Importantly, ADT-OH abrogates the accumulation of dysfunctional mitochondria and the subsequent cytosolic release of mitochondrial DNA in α-synuclein preformed fibrils (α-Syn PFF)-challenged microglia, thereby blunting the activation of the cGAS-STING pathway and the downstream production of inflammatory mediators. Furthermore, systemic administration of ADT-OH dampened microglial activation and cGAS expression in α-Syn-overexpressing PD mice, thereby mitigating the loss of midbrain dopaminergic neurons and ameliorating motor coordination deficits. Collectively, our findings demonstrate that ADT-OH exerts robust neuroprotective effects in PD models, both in vitro and in vivo, by enhancing mitophagy and inhibiting microglia-mediated neuroinflammation.
    Keywords:  ADT-OH; Parkinson’s disease; cGAS-STING; microglia; mitochondrial DNA; mitophagy
    DOI:  https://doi.org/10.1038/s41401-026-01789-7
  7. Circ Res. 2026 Apr 10. 138(8): e326988
    Rethinking Mitochondria: The Extracellular Dimension.
    Laura Pena-Couso, Magdalena Makuch, Jose Angel Nicolas-Avila.
      Mitochondria are essential organelles that transform the energy contained in metabolic substrates into ATP while supporting numerous cellular processes. Traditionally regarded as strictly intracellular, growing evidence now demonstrates that mitochondria and mitochondria-derived components can also be released into the extracellular space, giving rise to extracellular mitochondria. extracellular mitochondria display remarkable heterogeneity, ranging from intact organelles to individual molecular components, free to vesicle-encapsulated structures, and with functional states spanning from severely damaged to metabolically active. Their release is mediated by tightly regulated mechanisms in both living and dying cells, and is influenced by cellular stress, activation state, and pathways that control mitochondrial selection, compartmentalization, trafficking, and extrusion. Extracellular release fulfills multiple functions across the organism, including quality control, modulation of cellular identity, inflammatory signaling, and functional support of recipient cells. In the cardiovascular system, extracellular mitochondria contribute to both homeostasis and disease progression. This review summarizes current knowledge of extracellular mitochondria forms, mechanisms of release, and pathophysiological relevance, and highlights their emerging potential as therapeutic targets in cardiovascular pathophysiology and beyond.
    Keywords:  cardiovascular system; extracellular space; homeostasis; mitochondria; organelles
    DOI:  https://doi.org/10.1161/CIRCRESAHA.125.326988
  8. Cell Genom. 2026 Apr 08. pii: S2666-979X(26)00057-1. [Epub ahead of print]6(4): 101195
    A unified ACSF3-mtFAS model linking mitochondrial energy metabolism to human anthropometric evolution.
    Sara Tucci.
      We here propose a mitochondria-centered reinterpretation of the ACSF3 regulatory variant reported by Zhang et al., integrating advances in mitochondrial fatty acid synthesis and ACSF3-deficient models to link subcellular control of oxidative efficiency with organismal traits such as basal metabolic rate, height, and systemic growth regulation in humans.
    DOI:  https://doi.org/10.1016/j.xgen.2026.101195
  9. Curr Opin Neurol. 2026 Apr 07.
    Paroxysmal movement disorders: an update on genetics, mechanisms, and emerging therapeutic strategies.
    Maria Makrygianni, Robert Erro, Maria Stamelou.
       PURPOSE OF REVIEW: This review will discuss the latest genetic and pathophysiological spectrum of paroxysmal movement disorders and emerging therapeutic strategies.
    RECENT FINDINGS: Paroxysmal movement disorders comprise a heterogenous group of rare movement disorders characterized by intermittent episodes of spontaneous or triggered attacks of hyperkinetic movement disorders. Genetic spectrum has evolved offering new insights in the pathophysiological mechanisms of known genes as PRRT2 and new ones as TMEM151A. Also, SCA27B-related adult-onset cerebellar ataxia has emerged as a new treatable cause of episodic ataxia.
    SUMMARY: Exploring new pathophysiological associations can offer diagnostic precision and development of new therapeutic directions.
    Keywords:  episodic ataxia; parosymal kinesigenic dyskinesia; paroxysmal exercise-induced dyskinesia; paroxysmal nonkinesigenic dyskinesia
    DOI:  https://doi.org/10.1097/WCO.0000000000001495
  10. Medicine (Baltimore). 2026 Apr 10. 105(15): e48284
    Biomarkers in predicting mortality among ICU patients with sepsis.
    Sümeyye Uğur, Mustafa Kaçmaz.
      Sepsis is one of the most challenging conditions in intensive care units (ICUs), with an increased incidence and mortality, making it critical to predict both mortality and timing of resuscitation. This retrospective study aimed to analyze the association of a number of routinely used biomarkers with mortality in patients admitted to the ICU with sepsis. Patients >18 years of age, who had been admitted to the ICU with sepsis were included. At admission, baseline levels of C-reactive protein (CRP), procalcitonin (PCT), albumin and lactate, as well as white blood cell (WBC), neutrophil, and lymphocyte counts were recorded. The primary outcome was 28-day mortality. Of 235 patients (92 males; mean age 73.57 ± 13.63 years), 28-day mortality occurred in 113 patients (48.1%). The non-survivors differed significantly from survivors with higher WBC, neutrophil and lymphocyte counts, higher levels of PCT, CRP and lactate, and a lower albumin level (for all, P < .05). Mortality was associated with lactate, and inversely associated with albumin levels. In logistic regression analysis, albumin and lactate were risk factors to predict 28-day mortality, with odds ratios of 1.51 and 0.89, respectively. In receiver operating characteristic analysis, PCT, lactate and albumin had the greatest values for area under the curve (0.709, 0.654, and 0.696, respectively). Besides established but time-consuming and complicated scoring systems, lactate and albumin levels may be used to predict prognosis in ICU settings, with the advantage of ease in their availability.
    Keywords:  biomarkers; intensive care unit; mortality; sepsis
    DOI:  https://doi.org/10.1097/MD.0000000000048284
  11. Bone Res. 2026 Apr 07. pii: 40. [Epub ahead of print]14(1):
    Periosteal mitochondria DNA structures drive aging-associated poor skeletal repair.
    Yanlin Wu, Chuyi Han, Xue Yang, Yitian Wang, Weidong Tian, Quan Yuan, Hui Wang, Haisheng Wang, Bei Yin, Ling Ye, Feifei Li, Fanyuan Yu.
      Insufficient skeletal repair is the primary threat of health span and lifespan in elders with increasingly vast global burden; yet, to date, the knowledge of resolving this crisis remains limited. In this study, we addressed the specific mechanisms underlying aging-associated poor bone repair, which are driven by the mitochondrial DNA structures mitochondrial G-quadruplex (mtG4). We found that mtG4 is spatiotemporal-wisely accumulated within Pdgfra+ periosteal mesenchymal stromal/stem cells (PPM) both in healthy and premature aging, which substantially increases cellular senescence and the degenerative alterations of PPM. By utilizing transgenic lineage tracking, PPM organoids formation, mitochondrial transgenic mutation, organoids transplantation, and serial cellular molecular investigations, we reveal that mtG4 in PPM restricts vital mitochondrial genes' transcription to cause mitochondrial dysfunction, which utterly leads to severe mitophagy and cell senescence. These senescent PPM demonstrates impaired stemness and disrupted fate determination, finally phenocopying aging-associated poor bone repair. This study decodes the mitochondrial genomic reasons for insufficient bone repair during aging, which offers insights for developing cell-type- and disease-specific senolytic therapies in the future.
    DOI:  https://doi.org/10.1038/s41413-026-00524-6
  12. Front Aging Neurosci. 2026 ;18 1761702
    Mitochondrial dysfunction in Alzheimer's disease and related sex differences.
    Afzal Misrani, Conelius Ngwa, Fudong Liu.
      Alzheimer's disease (AD), the most common form of dementia, accounts for 70% of cases and remains a major healthcare challenge due to its rising prevalence and lack of disease-modifying treatments. Clinically, AD is a sexually dimorphic disease. Women exhibit more rapid cognitive decline and accelerated brain atrophy during mild cognitive impairment and early dementia, whereas men more frequently present cardiovascular comorbidities, earlier mitochondrial dysfunction, and greater neuropsychiatric symptoms. AD is marked by amyloid-β (Aβ) plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss, with mitochondrial dysfunction emerging as a key early contributor that exhibits sex specific phenotypes. Mitochondria are vital for neuronal function by generating ATP, maintaining calcium homeostasis, and regulating oxidative stress. However, mitochondria in AD exhibit impaired ATP synthesis, excessive reactive oxygen species (ROS) production, calcium dysregulation, and disrupted fission-fusion dynamics. AD mitochondrial dysfunction can be measured by molecular markers, such as increased expression of fission-related protein Drp1, decreased biogenesis regulator PGC-1α, and elevated oxidative stress markers like malonaldehyde, nitotyrosine and protein carbonyls. Accumulating data suggest that sex differences in mitochondrial dysfunction are attributed to either sex hormonal or sex chromosomal effects, which eventually contribute to sex dichotomic phenotypes of AD. This review collected data regarding mitochondrial dysfunction in AD, with an emphasis on sex differences in oxidative stress, energy metabolism, and regulatory pathways.
    Keywords:  Alzheimer's disease; dementia; mitochondria; oxidative stress; sex differences
    DOI:  https://doi.org/10.3389/fnagi.2026.1761702
  13. Circ Res. 2026 Apr 10. 138(8): e327357
    Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.
    Erjola Rapushi, Anubhav Aryal, Tianyuan Yang, Zhixin Li, Xiaohong Wang, Guo-Chang Fan.
      Mitochondria-derived vesicles (MDVs) and mitochondrial extracellular vesicles (mitoEVs) represent 2 related extensions of mitochondrial dynamics that link organelle maintenance to communication within and between cells. MDVs are small vesicles that bud directly from mitochondria, selectively packaging components of the outer membrane, inner membrane, or matrix. They serve as a localized quality control mechanism that removes oxidized or damaged material without engaging the entire mitophagic machinery. After budding, MDVs typically enter the endolysosomal pathway, where they can fuse with late endosomes or lysosomes for cargo degradation. A subset of MDVs also targets other organelles, particularly peroxisomes, contributing to organelle crosstalk, lipid metabolism, and redox balance. By contrast, mitoEVs released into the extracellular space contain intact functional mitochondria, mitochondrial contents (proteins, DNAs/RNAs, lipids, and so on), and nonmitochondrial cargo (ie, mRNAs, noncoding RNAs, and so on), which can be transferred to recipient cells and subsequently induce either pathogenic or beneficial outcomes. Therefore, mitoEVs have been implicated in metabolic cooperation, immune regulation, tissue remodeling, and aging. Accordingly, this review summarizes recent progress on the diverse mechanisms for the biogenesis of MDVs and mitoEVs, as well as available protocols for their isolation. The roles of MDVs and mitoEVs in mediating mitochondrial quality/quantity control and multiple layers of crosstalk between intracellular organelles and different cell types in health and disease are highlighted. Last, mitoEV-mediated pathogenic effects and therapeutic potential in cardiovascular disease are also discussed.
    Keywords:  cardiovascular diseases; extracellular vesicles; lipid metabolism; mitochondria; reactive oxygen species
    DOI:  https://doi.org/10.1161/CIRCRESAHA.125.327357
  14. Circ Res. 2026 Apr 10. 138(8): e326984
    Mitochondrial Transfer: From Bench to Bedside.
    Gentaro Ikeda, Jiwen Li, Alyssa Wang, Amogha Medha Paleru, Phillip C Yang.
      Intercellular mitochondrial transfer has emerged as a fundamental mechanism of tissue adaptation and repair in the cardiovascular system, with major implications for cardiovascular, neurological, metabolic, and inflammatory diseases. Once thought to be static, mitochondria are now recognized as mobile organelles that move between cells via tunneling nanotubes, extracellular vesicles, and free mitochondria. These pathways support 2 complementary axes of mitochondrial communication: Rescue by Replenish, in which healthy mitochondria or mitochondrial components restore bioenergetics and stress resistance in recipient cells, and Relief by Release, in which damaged mitochondria are exported for degradation to preserve homeostasis and limit inflammation. We summarize the molecular machinery governing tunneling nanotube formation, mitochondria-derived vesicle biogenesis, extracellular vesicle sorting, and free mitochondrial release and uptake, and discuss how these processes shape organ function. Building on these mechanistic insights, we outline 4 translational strategies: (1) cell-based therapies that donate healthy mitochondria or scavenge damaged ones; cell-free approaches using (2) mitochondria-containing extracellular vesicles or (3) purified mitochondria; (4) pharmacological, nutritional, and lifestyle interventions that augment endogenous mitochondrial turnover and intercellular exchange. Finally, we discuss key barriers to clinical translation, including inflammatory and oncogenic risks, mitonuclear incompatibility, incomplete understanding of the fate and durability of transferred mitochondria, and the lack of standardized manufacturing, potency assays, and long-term storage methods. Continued integration of mechanistic biology with bioengineering and regulatory science will be essential to safely move mitochondrial transfer-based therapies from bench to bedside in cardiovascular medicine.
    Keywords:  cell communication; energy metabolism; extracellular vesicles; homeostasis; inflammation; mitochondria; nanotubes
    DOI:  https://doi.org/10.1161/CIRCRESAHA.125.326984
  15. Chin Med. 2026 Apr 10. pii: 115. [Epub ahead of print]21(1):
    Moxibustion delays ovarian aging by regulating mitochondrial biogenesis and improving oocyte quality.
    Yaoli Yin, Yan Xu, Zemin Li, Meilin Chen, Ziwei Song, Hongxiao Li, Ge Lu, Meihong Shen.
       BACKGROUND: The growing trend of delayed childbearing in contemporary society has made fertility preservation a significant issue, prompting the search for diverse therapeutic options. Conversely, moxibustion is gaining increasing attention as a potential non-pharmacological therapy for supporting reproductive health.
    METHODS: Mice aged 2 to 14 months were assessed for ovarian function detection to determine the age of reproductive senescence and to identify the optimal time for moxibustion intervention to delay senescence. Oocyte quality and mitochondrial function assessments were conducted to investigate the role of mitochondrial biogenesis in ovarian aging and the underlying mechanisms following moxibustion intervention.
    RESULTS: Mice aged 10 months demonstrated ovarian dysfunction associated with aging. Moxibustion significantly elevated hormone levels, increased the number of growing follicles, enhanced embryo implantation and viable birth rates, and reduced embryonic mortality in aging mice. The most pronounced effects were observed in 10-month-old mice. These beneficial outcomes might be linked to improved oocyte quality. Crucially, moxibustion positively increased mitochondrial quantity, enhanced mitochondrial quality, and influenced mitochondrial biogenesis, an effect comparable to that of the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) agonist valproic acid. Furthermore, the beneficial effects of moxibustion were partially attenuated by a PGC-1α inhibitor.
    CONCLUSIONS: Moxibustion, as a non-pharmacological intervention, may mitigate ovarian aging and serve as an effective therapeutic strategy for extending human fertility.
    Keywords:  Mitochondrial biogenesis; Moxibustion; Oocyte; Ovarian aging
    DOI:  https://doi.org/10.1186/s13020-026-01375-3
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