bims-mitrat Biomed News
on Mitochondrial transplantation and transfer
Issue of 2024–12–22
thirteen papers selected by
Gökhan Burçin Kubat, Gulhane Health Sciences Institute
  1. Acute treadmill exercise induces mitochondrial unfolded protein response in skeletal muscle of male rats.
  2. Exercise as Mitochondrial Medicine: How Does the Exercise Prescription Affect Mitochondrial Adaptations to Training?
  3. Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation.
  4. Impact of exercise and fasting on mitochondrial regulators in human muscle.
  5. Aging promotes an increase in mitochondrial fragmentation in astrocytes.
  6. Mitochondrial transfer of drug-loaded artificial mitochondria for enhanced anti-Glioma therapy through synergistic apoptosis/ferroptosis/immunogenic cell death.
  7. Wnt7a is required for regeneration of dystrophic skeletal muscle.
  8. Exploring the role and application of mitochondria in radiation therapy.
  9. Mitochondrial respiration atlas reveals differential changes in mitochondrial function across sex and age.
  10. Mitochondrial metabolism and epigenetic crosstalk drive the SASP.
  11. Biodistribution of therapeutic extracellular vesicles.
  12. Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon.
  13. Quercetin preserves mitochondria-endoplasmic reticulum contact sites improving mitochondrial dynamics in aged myocardial cells.
  1. Biochim Biophys Acta Bioenerg. 2024 Dec 13. pii: S0005-2728(24)00502-4. [Epub ahead of print]1866(2): 149532
    Acute treadmill exercise induces mitochondrial unfolded protein response in skeletal muscle of male rats.
    Ibrahim Turkel, Gokhan Burcin Kubat, Tugba Fatsa, Ozgu Acet, Berkay Ozerklig, Burak Yazgan, Gulcin Simsek, Keshav K Singh, Sukran Nazan Kosar.
      Mitochondria are often referred to as the energy centers of the cell and are recognized as key players in signal transduction, sensing, and responding to internal and external stimuli. Under stress conditions, the mitochondrial unfolded protein response (UPRmt), a conserved mitochondrial quality control mechanism, is activated to maintain mitochondrial and cellular homeostasis. As a physiological stimulus, exercise-induced mitochondrial perturbations trigger UPRmt, coordinating mitochondria-to-nucleus communication and initiating a transcriptional program to restore mitochondrial function. The aim of this study was to evaluate the UPRmt signaling response to acute exercise in skeletal muscle. Male rats were subjected to acute treadmill exercise at 25 m/min for 60 min on a 0 % grade. Plantaris muscles were collected from both sedentary and exercise groups at various times: immediately (0), and at 1, 3, 6, 12, and 24 h post-exercise. Reactive oxygen species (ROS) production was assessed using hydrogen peroxide assay and dihydroethidium staining. Additionally, the mRNA and protein expression of UPRmt markers were measured using ELISA and real-time PCR. Mitochondrial activity was assessed using succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) staining. Our results demonstrated that acute exercise increased ROS production and upregulated UPRmt markers at both gene and protein levels. Moreover, skeletal muscle exhibited an increase in mitochondrial activity in response to exercise, as indicated by SDH and COX staining. These findings suggest that acute treadmill exercise is sufficient to induce ROS production, activate UPRmt signaling, and enhance mitochondrial activity in skeletal muscle, expanding our understanding of mitochondrial adaptations to exercise.
    Keywords:  Exercise; Mitochondria; Mitochondrial proteostasis; Mitochondrial unfolded protein response; Skeletal muscle; UPR(mt)
    DOI:  https://doi.org/10.1016/j.bbabio.2024.149532
  2. Annu Rev Physiol. 2024 Dec 10.
    Exercise as Mitochondrial Medicine: How Does the Exercise Prescription Affect Mitochondrial Adaptations to Training?
    David J Bishop, Matthew J-C Lee, Martin Picard.
      Mitochondria are multifaceted organelles with several life-sustaining functions beyond energy transformation, including cell signaling, calcium homeostasis, hormone synthesis, programmed cell death (apoptosis), and others. A defining aspect of these dynamic organelles is their remarkable plasticity, which allows them to sense, respond, and adapt to various stressors. In particular, it is well-established that the stress of exercise provides a powerful stimulus that can trigger transient or enduring changes to mitochondrial molecular features, activities, integrated functions, behaviors, and cell-dependent mitochondrial phenotypes. Evidence documenting the many beneficial mitochondrial adaptations to exercise has led to the notion of exercise as a mitochondrial medicine. However, as with other medicines, it is important to understand the optimal prescription (i.e., type, dose, frequency, duration). In this review, we build on a systematic biological framework that distinguishes between domains of mitochondrial biology to critically evaluate how different exercise prescription variables influence mitochondrial adaptations to training.
    DOI:  https://doi.org/10.1146/annurev-physiol-022724-104836
  3. Int J Mol Sci. 2024 Nov 28. pii: 12783. [Epub ahead of print]25(23):
    Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation.
    Seo-Eun Lee, Shin-Hye Yu, In-Hyeon Kim, Young Cheol Kang, Yujin Kim, Jeong Seon Yeo, Jun Hyeok Lim, Iksun Kwon, Je-Hein Kim, Se-Woong Park, Mi-Yoon Chang, Kyuboem Han, Sung-Hwan Kim, Chun-Hyung Kim.
      Idiopathic pulmonary fibrosis (IPF) is a pulmonary disease characterized by excessive extracellular matrix protein deposition in the lung interstitium, subsequently causing respiratory failure. IPF still has a high medical unmet requirement due to the lack of effective treatments to inhibit disease progression. The etiology of IPF remains unclear, but mitochondrial dysfunction is considered to be associated with IPF development. Therefore, targeting mitochondrial abnormalities would be a promising strategy for treating IPF. Recently, exogenous mitochondrial transplantation has been beneficial for treating mitochondrial dysfunction. The current study aimed to examine the therapeutic effect of mitochondrial transplantation on IPF in vitro and in vivo. Mitochondria were isolated from human umbilical cord mesenchymal stem cells, referred to as PN-101. Human lung fibroblasts and human bronchial epithelial cells were exposed to transforming growth factor-β, followed by PN-101 treatment to determine the in vitro efficacy of mitochondrial transplantation. An IPF mouse model established by a single intratracheal instillation of bleomycin was utilized to determine the in vivo efficacy of the intravenously treated mitochondria. PN-101 attenuated mitochondrial damage, inhibited EMC production, and suppressed epithelial-to-mesenchymal transition in vitro. Additionally, intravenous PN-101 administration alleviated bleomycin-induced fibrotic processes in the IPF mouse model with a therapeutic context. Our data indicate that PN-101 is a novel and potential therapeutic agent for IPF.
    Keywords:  anti-inflammation; antiapoptosis; idiopathic pulmonary fibrosis (IPF); mitochondria; stem cell; transplantation
    DOI:  https://doi.org/10.3390/ijms252312783
  4. Transl Exerc Biomed. 2024 Sep;1(3-4): 183-194
    Impact of exercise and fasting on mitochondrial regulators in human muscle.
    Eveline S Menezes, Hashim Islam, Benjamin B Arhen, Craig A Simpson, Chris McGlory, Brendon J Gurd.
       Objectives: To investigate the impact of acute energetic stress (acute HIIE and fasting) on ERRγ, PPARβ, NR1D1, NR4A1, and TFEB in human skeletal muscle.
    Methods: The current study performed secondary analyses using muscle biopsy samples from two previously published studies: study 1) leg muscle biopsies from nine men and eight women were obtained pre and 3 h following acute high-intensity interval cycling exercise (HIIE); study 2) leg muscle biopsies were obtained from nine men pre-, during, and post-an 8 h fast with or without 2 h of arm ergometer exercise. RT-PCR was performed on samples from each study to determine the mRNA expression of ERRγ, PPARβ, NR1D1, NR4A1, and TFEB. Additionally, we retrieved data from meta-analyzed human muscle gene expression using the publicly available database MetaMex.
    Results: PGC-1α (p<0.01, d=1.98) and NR4A1 (p<0.01, d=1.36) mRNA expression significantly increased while TFEB (p≤0.05, d=0.70) decreased following HIIE. Significant decreases in NR4A1 and NR1D1 mRNA expression were observed following an 8 h fast. Our MetaMex analyses revealed significant increases (p<0.05) in PGC-1α and NR4A1 expression following aerobic and resistance exercise, and in PPARβ expression following resistance exercise.
    Conclusions: Our data indicate that acute HIIE stimulates increases in NR4A1 and PGC-1α and decreases in TFEB mRNA expression in human skeletal muscle. Additionally, a short term (8 h) fast reduced the mRNA expression of the transcriptional regulators NR4A1 and NR1D1 - potentially as a mechanism of decreasing mitochondrial biogenesis to reduce energy expenditure during a period of restricted energy availability.
    Keywords:  aerobic exercise; caloric restriction; food deprivation; muscle remodeling; transcriptional regulators
    DOI:  https://doi.org/10.1515/teb-2024-0014
  5. Front Cell Neurosci. 2024 ;18 1496163
    Aging promotes an increase in mitochondrial fragmentation in astrocytes.
    Ana Paula Bergamo Araujo, Gabriele Vargas, Lívia de Sá Hayashide, Isadora Matias, Cherley Borba Vieira Andrade, Jorge José de Carvalho, Flávia Carvalho Alcantara Gomes, Luan Pereira Diniz.
       Introduction: Brain aging involves a complex interplay of cellular and molecular changes, including metabolic alterations and the accumulation of senescent cells. These changes frequently manifest as dysregulation in glucose metabolism and mitochondrial function, leading to reduced energy production, increased oxidative stress, and mitochondrial dysfunction-key contributors to age-related neurodegenerative diseases.
    Methods: We conducted experiments on two models: young (3-4 months) and aged (over 18 months) mice, as well as cultures of senescent and control mouse astrocytes. Mitochondrial content and biogenesis were analyzed in astrocytes and neurons from aged and young animals. Cultured senescent astrocytes were examined for mitochondrial membrane potential and fragmentation. Quantitative PCR (qPCR) and immunocytochemistry were used to measure fusion- and fission-related protein levels. Additionally, transmission electron microscopy provided morphological data on mitochondria.
    Results: Astrocytes and neurons from aged animals showed a significant reduction in mitochondrial content and a decrease in mitochondrial biogenesis. Senescent astrocytes in culture exhibited lower mitochondrial membrane potential and increased mitochondrial fragmentation. qPCR and immunocytochemistry analyses revealed a 68% increase in fusion-related proteins (mitofusin 1 and 2) and a 10-fold rise in DRP1, a key regulator of mitochondrial fission. Transmission electron microscopy showed reduced perimeter, area, and length-to-diameter ratio of mitochondria in astrocytes from aged mice, supported by elevated DRP1 phosphorylation in astrocytes of the cerebral cortex.
    Discussion: Our findings provide novel evidence of increased mitochondrial fragmentation in astrocytes from aged animals. This study sheds light on mechanisms of astrocytic metabolic dysfunction and mitochondrial dysregulation in brain aging, highlighting mitochondrial fragmentation as a potential target for therapeutic interventions in age-related neurodegenerative diseases.
    Keywords:  astrocytes; brain aging; mitochondrial biogenesis and neurodegeneration; mitochondrial dysfunction; mitochondrial fragmentation
    DOI:  https://doi.org/10.3389/fncel.2024.1496163
  6. Acta Biomater. 2024 Dec 12. pii: S1742-7061(24)00738-4. [Epub ahead of print]
    Mitochondrial transfer of drug-loaded artificial mitochondria for enhanced anti-Glioma therapy through synergistic apoptosis/ferroptosis/immunogenic cell death.
    Mingzhu Song, Jiayu Yuan, Ge Zhang, Mengdi Sun, Yifei Zhang, Xiangchen Su, Ruizhen Lv, Yuting Zhao, Yijie Shi, Liang Zhao.
      Mitochondrial targeting in gliomas represents a novel therapeutic strategy with significant potential to enhance drug sensitivity by effectively leveraging the inherent vulnerabilities of glioma cells at the mitochondrial level. In this study, we developed a sophisticated nano-delivery system by engineering artificial mitochondria from mitochondrial membrane-based nanovesicles, enabling precise targeting of doxorubicin (Dox) to selectively eradicate cancer cells while amplifying multiple cell death pathways. It was found that Dox-encapsulating mitochondria-based nanovesicles (DOX-MitoNVs) have exhibited an extraordinary ability to penetrate the blood-brain barrier (BBB), specifically targeting gliomas. By targeting mitochondria instead of infiltrating the nucleus, DOX-MitoNVs not only amplified Dox mediated apoptosis effects through the overload of intracellular Ca2+ but also intensified ferroptosis by generating reactive oxygen species (ROS). Furthermore, DOX-MitoNVs demonstrated a significant ability to modulate the tumor immune microenvironment, thereby inducing pronounced immunogenic cell death (ICD) effects. In summary, it presents a novel therapeutic strategy utilizing DOX-MitoNVs for precise mitochondrial targeting in gliomas, enhancing drug sensitivity, inducing multiple cell death pathways, and modulating the tumor immune microenvironment to promote immunogenic cell death. STATEMENT OF SIGNIFICANCE: Mitochondrial targeting in gliomas is a promising therapeutic strategy that enhances drug sensitivity by exploiting glioma cells' mitochondrial vulnerabilities. We engineered artificial mitochondria from mitochondrial membrane-based nanovesicles as a novel nano-delivery system for precise targeting of Doxorubicin (Dox). This approach facilitates selective cancer cell eradication and amplifies multiple cell death pathways alongside immunogenic chemotherapy. Notably, Dox-encapsulating mitochondria-based nanovesicles (DOX-MitoNVs) effectively cross the blood-brain barrier (BBB) and specifically target gliomas. By focusing on mitochondria, Dox induces apoptosis and intensifies ferroptosis through reactive oxygen species (ROS) generation. Additionally, DOX-MitoNVs can transform the tumor immune microenvironment, promoting immunogenic cell death (ICD). Overall, DOX-MitoNVs offer a compelling platform for enhanced glioma therapy.
    Keywords:  ICD; Mitochondria; apoptosis; doxorubicin; ferroptosis; nanovesicles
    DOI:  https://doi.org/10.1016/j.actbio.2024.12.027
  7. Skelet Muscle. 2024 Dec 19. 14(1): 34
    Wnt7a is required for regeneration of dystrophic skeletal muscle.
    Uxia Gurriaran-Rodriguez, Kasun Kodippili, David Datzkiw, Ehsan Javandoost, Fan Xiao, Maria Teresa Rejas, Michael A Rudnicki.
      Intramuscular injection of Wnt7a has been shown to accelerate and augment skeletal muscle regeneration and to ameliorate dystrophic progression in mdx muscle, a model for Duchenne muscular dystrophy (DMD). Here, we assessed muscle regeneration and function in wild type (WT) and mdx mice where Wnt7a was deleted in muscle using a conditional Wnt7a floxed allele and a Myf5-Cre driver. We found that both WT and mdx mice lacking Wnt7a in muscle, exhibited marked deficiencies in muscle regeneration at 21 d following cardiotoxin (CTX) induced injury. Unlike WT, deletion of Wnt7a in mdx resulted in decreased force generation prior to CTX injury. However, both WT and mdx muscle lacking Wnt7a displayed decreased force generation following CTX injection. Notably the regeneration deficit in mdx mice was rescued by a single tail vein injection of extracellular vesicles containing Wnt7a (Wnt7a-EVs). Therefore, we conclude that the regenerative capacity of muscle in mdx mice is highly dependant on the upregulation of endogenous Wnt7a following injury, and that systemic delivery of Wnt7a-EVs represents a therapeutic strategy for treating DMD.
    Keywords:  Duchenne muscular dystrophy; Regeneration, Wnt7a, Extracellular vesicles; Skeletal muscle
    DOI:  https://doi.org/10.1186/s13395-024-00367-x
  8. Biochim Biophys Acta Mol Basis Dis. 2024 Dec 12. pii: S0925-4439(24)00617-3. [Epub ahead of print] 167623
    Exploring the role and application of mitochondria in radiation therapy.
    Yi Ding, Wang Jing, Zhichao Kang, Zhe Yang.
      Mitochondria are pivotal in cellular energy metabolism, the oxidative stress response and apoptosis. Recent research has focused on harnessing their functions to enhance the efficacy of radiation therapy (RT). This review focuses on the critical functions and applications of mitochondria in radiation therapy, including the targeting of mitochondrial metabolism and the modulation of mitochondria-mediated cell death and immune responses. While these strategies have demonstrated considerable potential in preclinical studies to improve radiotherapy outcomes, challenges remain, such as optimizing drug delivery systems, ensuring safety and overcoming resistance to therapy.
    Keywords:  Mitochondria; Mitochondrial metabolic reprogramming; Radiotherapy
    DOI:  https://doi.org/10.1016/j.bbadis.2024.167623
  9. Elife. 2024 Dec 20. pii: RP96926. [Epub ahead of print]13
    Mitochondrial respiration atlas reveals differential changes in mitochondrial function across sex and age.
    Dylan C Sarver, Muzna Saqib, Fangluo Chen, G William Wong.
      Organ function declines with age, and large-scale transcriptomic analyses have highlighted differential aging trajectories across tissues. The mechanism underlying shared and organ-selective functional changes across the lifespan, however, still remains poorly understood. Given the central role of mitochondria in powering cellular processes needed to maintain tissue health, we therefore undertook a systematic assessment of respiratory activity across 33 different tissues in young (2.5 months) and old (20 months) mice of both sexes. Our high-resolution mitochondrial respiration atlas reveals: (1) within any group of mice, mitochondrial activity varies widely across tissues, with the highest values consistently seen in heart, brown fat, and kidney; (2) biological sex is a significant but minor contributor to mitochondrial respiration, and its contributions are tissue-specific, with major differences seen in the pancreas, stomach, and white adipose tissue; (3) age is a dominant factor affecting mitochondrial activity, especially across most brain regions, different fat depots, skeletal muscle groups, eyes, and different regions of the gastrointestinal tract; (4) age effects can be sex- and tissue-specific, with some of the largest effects seen in pancreas, heart, adipose tissue, and skeletal muscle; and (5) while aging alters the functional trajectories of mitochondria in a majority of tissues, some are remarkably resilient to age-induced changes. Altogether, our data provide the most comprehensive compendium of mitochondrial respiration and illuminate functional signatures of aging across diverse tissues and organ systems.
    Keywords:  aging; computational biology; mitochondria; mouse; respiration atlas; sex; systems biology
    DOI:  https://doi.org/10.7554/eLife.96926
  10. Res Sq. 2024 Dec 05. pii: rs.3.rs-5278203. [Epub ahead of print]
    Mitochondrial metabolism and epigenetic crosstalk drive the SASP.
    Joao Passos, Helene Martini, Jodie Birch, Francisco Marques, Stella Victorelli, Anthony Lagnado, Nicholas Pirius, Ana Franco, Gung Lee, Yeaeun Han, Jennifer Rowsey, Alexandre Gaspar-Maia, Aaron Havas, Rabi Murad, Xue Lei, Rebecca Porritt, Oliver Maddocks, Diana Jurk, Sundeep Khosla, Peter Adams.
      Senescent cells drive tissue dysfunction through the senescence-associated secretory phenotype (SASP). We uncovered a central role for mitochondria in the epigenetic regulation of the SASP, where mitochondrial-derived metabolites, specifically citrate and acetyl-CoA, fuel histone acetylation at SASP gene loci, promoting their expression. We identified the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY) as critical for this process. Inhibiting these pathways selectively suppresses SASP without affecting cell cycle arrest, highlighting their potential as therapeutic targets for age-related inflammation. Notably, SLC25A1 inhibition reduces systemic inflammation and extends healthspan in aged mice, establishing mitochondrial metabolism as pivotal to the epigenetic control of aging.
    DOI:  https://doi.org/10.21203/rs.3.rs-5278203/v1
  11. Extracell Vesicles Circ Nucl Acids. 2023 ;4(2): 170-190
    Biodistribution of therapeutic extracellular vesicles.
    Dhanu Gupta, Oscar P B Wiklander, Matthew J A Wood, Samir El-Andaloussi.
      The field of extracellular vesicles (EVs) has seen a tremendous paradigm shift in the past two decades, from being regarded as cellular waste bags to being considered essential mediators in intercellular communication. Their unique ability to transfer macromolecules across cells and biological barriers has made them a rising star in drug delivery. Mounting evidence suggests that EVs can be explored as efficient drug delivery vehicles for a range of therapeutic macromolecules. In contrast to many synthetic delivery systems, these vesicles appear exceptionally well tolerated in vivo. This tremendous development in the therapeutic application of EVs has been made through technological advancement in labelling and understanding the in vivo biodistribution of EVs. Here in this review, we have summarised the recent findings in EV in vivo pharmacokinetics and discussed various biological barriers that need to be surpassed to achieve tissue-specific delivery.
    Keywords:  CNS targeting; Exosomes; extracellular vesicles; in vivo biodistribution; targeted delivery
    DOI:  https://doi.org/10.20517/evcna.2023.12
  12. Front Cell Neurosci. 2024 ;18 1509283
    Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon.
    Tom Venneman, Pieter Vanden Berghe.
      Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium. Elevated Ca2+ levels have been demonstrated to inhibit mitochondrial transport in many cell types, including neurons. However, it is currently unclear to what extent calcium-signaling regulates axonal mitochondrial transport during realistic neuronal activity patterns. We created a robust pipeline to quantify with high spatial resolution, absolute Ca2+ concentrations. This allows us to monitor Ca2+ dynamics with pixel precision in the axon and other neuronal compartments. We found that axonal calcium levels scale with firing frequency in the range of 0.1-1 μM, whereas KCl-induced depolarization generated levels almost a magnitude higher. As expected, prolonged KCl-induced depolarization did inhibit axonal mitochondrial transport in primary hippocampal neurons. However, physiologically relevant neuronal activity patterns only inhibited mitochondrial transport in axonal segments which made connections to a target neuron. In "non-connecting" axonal segments, we were unable to trigger this inhibitory mechanism using realistic firing patterns. Thus, we confirm that neuronal activity can indeed regulate axonal mitochondrial transport, and reveal a spatial pattern to this regulation which went previously undetected. Together, these findings indicate a potent, but localized role for activity-related calcium fluctuations in the regulation of axonal mitochondrial transport.
    Keywords:  axonal mitochondrial transport; neuronal activity; ratiometric calcium imaging; synaptic connections; transport regulation
    DOI:  https://doi.org/10.3389/fncel.2024.1509283
  13. Biogerontology. 2024 Dec 20. 26(1): 29
    Quercetin preserves mitochondria-endoplasmic reticulum contact sites improving mitochondrial dynamics in aged myocardial cells.
    Ray Jiménez, Alejandra Zúñiga-Muñoz, Edith Álvarez-León, Wylly Ramsés García-Niño, Gabriela Navarrete-Anastasio, Elizabeth Soria-Castro, Israel Pérez-Torres, Elizabeth Lira-Silva, Natalia Pavón, Alfredo Cruz-Gregorio, Rebeca López-Marure, Cecilia Zazueta, Alejandro Silva-Palacios.
      Cardiomyocyte senescence plays a crucial role in the pathophysiology of age-related cardiovascular disease. Senescent cells with impaired contractility, mitochondrial dysfunction, and hypertrophic growth accumulate in the heart during aging, contributing to cardiac dysfunction and remodeling. Mitochondrial dynamics is altered in aging cells, leading to changes in their function and morphology. Such rearrangements can affect the spatially restricted region of the mitochondrial membrane that interacts with reticulum membrane fragments, termed mitochondria-endoplasmic reticulum (ER) contact sites (MERCs). Besides, oxidative stress associated with inefficient organelle turnover can drive cellular senescence. Therefore, in this study, we evaluated the possible association between the senolytic effect of the antioxidant quercetin (Q) and MERCs preservation in a D-galactose-induced cellular senescence model. We found that Q ameliorates the senescent phenotype of H9c2 cells in association with increased mitochondria-ER colocalization, reduced distance between both organelles, and lower ROS production. Moreover, regulation of fusion and fission processes was related with increased mitochondrial ATP production and enhanced transmembrane potential. Overall, our data provide evidence that the inhibitory effect of Q on cellular senescence is associated with preserved MERCs and improved mitochondrial function and morphology, which might contribute to the attenuation of cardiac dysfunction.
    Keywords:  Cardiac senescence; Mitochondria-endoplasmic reticulum contact sites; Mitochondrial dynamic; Quercetin; Senolysis
    DOI:  https://doi.org/10.1007/s10522-024-10174-y
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