MitochondrionPub Date : 2024-03-17DOI: 10.1016/j.mito.2024.101873
Dilpreet Singh
{"title":"Revolutionizing cellular energy: The convergence of mitochondrial dynamics and delivery technologies","authors":"Dilpreet Singh","doi":"10.1016/j.mito.2024.101873","DOIUrl":"10.1016/j.mito.2024.101873","url":null,"abstract":"<div><p>The intersection of mitochondrial dynamics and delivery technologies heralds a paradigm shift in cellular biology and therapeutic intervention. Mitochondrial dynamics, encompassing fusion, fission, transport, and mitophagy, are critical for cellular energy production, signaling, and homeostasis. Dysregulation of these processes is implicated in a myriad of diseases, including neurodegenerative disorders, cardiovascular diseases, and cancer. Concurrently, advances in delivery technologies, such as nanocarriers, targeted delivery systems, and gene editing tools, offer unprecedented opportunities to manipulate mitochondrial function directly. This review synthesizes current knowledge on mitochondrial dynamics, examines recent breakthroughs in targeted delivery methods, and explores their potential convergence to modulate cellular energetics for therapeutic purposes. By integrating insights from biology, chemistry, and bioengineering, this review highlights the innovative approaches being developed to enhance mitochondrial function, underscoring the potential of this convergence to address complex diseases. This interdisciplinary perspective not only broadens our understanding of cellular processes but also paves the way for novel therapeutic strategies, marking a significant step forward in the quest for precision medicine and targeted interventions in mitochondrial-related diseases.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101873"},"PeriodicalIF":4.4,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140154387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-03-17DOI: 10.1016/j.mito.2024.101872
Lucio Della Guardia , Livio Luzi , Roberto Codella
{"title":"Muscle-UCP3 in the regulation of energy metabolism","authors":"Lucio Della Guardia , Livio Luzi , Roberto Codella","doi":"10.1016/j.mito.2024.101872","DOIUrl":"10.1016/j.mito.2024.101872","url":null,"abstract":"<div><p>Uncoupling protein-3 (UCP3) is a mitochondria-regulatory protein with potential energy- homeostatic functions. This study explores the role of UCP3 in the regulation of muscle- and energy metabolism. UCP3 is critical for tuning substrate utilization, favoring lipid oxidation, particularly in conditions of high-fat availability. While UCP3 is non-essential for lipid oxidation during energy excess, it proves vital during fasting, indicating an energy-homeostatic trait. Preliminary evidence indicates UCP3′ promotion of glucose uptake and oxidation, at least in conditions of high glucose/low fat availability. However, the dynamics of how fats and glucose differentially influence UCP3 remain undefined. UCP3 exhibits inducible proton transport and uncoupling activity, operating in a dual manner: <em>a resting state</em> with no/low activity and an <em>activated state</em> in the presence of activators. Uncoupling may enhance thermogenesis in specific conditions and in the presence of activators such as fatty acids, thyroid hormones, and catecholamines. This energy-dissipative activity adapts to varying energy availability, balancing energy dissipation with fatty acid oxidation to optimize whole-body energy homeostasis: fasting triggers UCP3 upregulation, enhancing lipid utilization while suppressing uncoupling. Additionally, UCP3 upregulation induces glucose and lipid disposal from the bloodstream and decreases tri-/diglyceride storage in muscle. This process improves mitochondrial functionality and insulin signaling, leading to enhanced systemicgluco-metabolic balance and protection from metabolic conditions. Reviewed evidence suggests that UCP3 plays a crucial role in adapting the system to changing energy conditions. However, the precise role of UCP3 in regulating metabolism requires further elucidation.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101872"},"PeriodicalIF":4.4,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1567724924000308/pdfft?md5=b9cf4ea62045af8399b7135bce3d52ba&pid=1-s2.0-S1567724924000308-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140154385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-03-16DOI: 10.1016/j.mito.2024.101875
Zecheng Liu , Ting Jin , Bingxin Qin , Rongrong Li , Jinjie Shang , Ying Huang
{"title":"The deletion of ppr2 interferes iron sensing and leads to oxidative stress response in Schizosaccharomyces pombe","authors":"Zecheng Liu , Ting Jin , Bingxin Qin , Rongrong Li , Jinjie Shang , Ying Huang","doi":"10.1016/j.mito.2024.101875","DOIUrl":"10.1016/j.mito.2024.101875","url":null,"abstract":"<div><p>Pentatricopeptide repeat proteins are involved in mitochondrial both transcriptional and posttranscriptional regulation. <em>Schizosaccharomyces pombe</em> Ppr2 is a general mitochondrial translation factor that plays a critical role in the synthesis of all mitochondrial DNA-encoded oxidative phosphorylation subunits, which are essential for mitochondrial respiration. Our previous analysis showed that <em>ppr2</em> deletion resulted in increased expression of iron uptake genes and caused ferroptosis-like cell death in <em>S. pombe</em>. In the present work, we showed that deletion of <em>ppr2</em> reduced viability on glycerol- and galactose-containing media.<!--> <!-->Php4 is a transcription repressor that regulates iron homeostasis in fission yeast. We found that in the <em>ppr2</em> deletion strain, Php4 was constitutively active and accumulated in the nucleus in the stationary phase. We also found that deletion of <em>ppr2</em> decreased the ferroptosis-related protein Gpx1 in the mitochondria. Overexpression of Gpx1 improves the viability of Δ<em>ppr2</em> cells. We showed that the deletion of <em>ppr2</em> increased the production of ROS, downregulated heme synthesis and iron-sulfur cluster proteins, and induced stress proteins. Finally, we observed the nuclear accumulation of Pap1-GFP and Sty1-GFP, suggesting that Sty1 and Pap1 in response to cellular stress in the <em>ppr2</em> deletion strain. These results suggest that<!--> <em>ppr2</em> deletion may cause mitochondrial dysfunction, which is likely to lead to iron-sensing defect and iron starvation response, resulting in perturbation of iron homeostasis and increased hydroxyl radical production. The increased hydroxyl radical production triggers cellular responses in the<!--> <em>ppr2</em> deletion strain.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101875"},"PeriodicalIF":4.4,"publicationDate":"2024-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140154313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-03-11DOI: 10.1016/j.mito.2024.101869
M. Montserrat-Mesquida , M.D. Ferrer , A. Pons , A. Sureda , X. Capó
{"title":"Effects of chronic hydrogen peroxide exposure on mitochondrial oxidative stress genes, ROS production and lipid peroxidation in HL60 cells","authors":"M. Montserrat-Mesquida , M.D. Ferrer , A. Pons , A. Sureda , X. Capó","doi":"10.1016/j.mito.2024.101869","DOIUrl":"10.1016/j.mito.2024.101869","url":null,"abstract":"<div><p>Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is a reactive species that is also involved in the redox regulation of cells because of it is relative stability. In numerous pathological situations, a chronic increase in the production of reactive species is observed, which is related to oxidative stress and cellular damage. This study aimed to evaluate the effects of long-term exposure to different H<sub>2</sub>O<sub>2</sub> concentrations on oxidative stress biomarkers and mitochondrial dynamics in HL60 cells. HL60 cells were treated with a sustained production (0.1, 1.0 and 10.0 nM/s) of H<sub>2</sub>O<sub>2</sub> for one hour. H<sub>2</sub>O<sub>2</sub> production and malondialdehyde (MDA) levels, as a lipid peroxidation marker, increased progressively in HL60 cells in accordance with higher H<sub>2</sub>O<sub>2</sub> exposure, with significant differences between the 10 nM/s H<sub>2</sub>O<sub>2</sub> group and the control and 0.1 nM/s groups. Similarly, progressive increased expression in genes related to the mitochondrial antioxidant defences and mitochondrial dynamics were also observed. Significantly increased gene expression in the 10 nM/s H<sub>2</sub>O<sub>2</sub> with respect to the control group was observed for manganese superoxide dismutase (MnSOD), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG1α), nuclear respiratory factor 2 (Nrf2), mitochondrial transcription factor A (Tfam), mitofusins 1 and 2 (Mfn1 and Mfn2) and uncoupling protein 3 (UCP3), whereas no significant changes were observed in the cytochrome <em>c</em> oxidase subunit IV (COXIV) gene expression. In conclusion, exposure to different sustained production of H<sub>2</sub>O<sub>2</sub> is related to a progressive increase in the gene expression of mitochondrial dynamics and redox processes in HL60 cells, but also to oxidative damage at higher H<sub>2</sub>O<sub>2</sub> production levels.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101869"},"PeriodicalIF":4.4,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140099890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-03-11DOI: 10.1016/j.mito.2024.101870
Debolina Saha , Sonam Kothari , Shilpa Duttaprasanna Kulkarni , Menaka Thambiraja , Ragothaman M Yennamalli , Dhanjit K Das
{"title":"Genetic heterogeneity and respiratory chain enzyme analysis in pediatric Indian patients with mitochondrial disorder: Report of novel variants in POLG1 gene and their functional implication using molecular dynamic simulation","authors":"Debolina Saha , Sonam Kothari , Shilpa Duttaprasanna Kulkarni , Menaka Thambiraja , Ragothaman M Yennamalli , Dhanjit K Das","doi":"10.1016/j.mito.2024.101870","DOIUrl":"10.1016/j.mito.2024.101870","url":null,"abstract":"<div><p>Mitochondrial disorders are a heterogeneous group of disorders caused by mutations in the mitochondrial DNA or in nuclear genes encoding the mitochondrial proteins and subunits. Polymerase Gamma (POLG) is a nuclear gene and mutation in the POLG gene are one of the major causes of inherited mitochondrial disorders. In this study, 15 pediatric patients, with a wide spectrum of clinical phenotypes were screened using blood samples (n = 15) and muscle samples (n = 4). Respiratory chain enzyme analysis in the muscle samples revealed multi-complex deficiencies with Complex I deficiency present in (1/4) patients, Complex II (2/4), Complex III (3/4) and Complex IV (2/4) patients. Multiple large deletions were observed in 4/15 patients using LR-PCR. Whole exome sequencing (WES) revealed a compound heterozygous mutation consisting of a POLG1 novel variant (NP_002684.1:p.Trp261X) and a missense variant (NP_002684.1:p. Leu304Arg) in one patient and another patient harboring a novel homozygous POLG1 variant (NP_002684.1:p. Phe750Val). These variants (NP_002684.1:p. Leu304Arg) and (NP_002684.1:p. Phe750Val) and their interactions with DNA were modelled using molecular docking and molecular dynamics (MD) simulation studies. The protein conformation was analyzed as root mean square deviation (RMSD), root mean square fluctuation (RMSF) which showed local fluctuations in the mutants compared to the wildtype. However, Solvent Accessible Surface Area (SASA) significantly increased for NP_002684.1:p.Leu304Arg and decreased in NP_002684.1:p.Phe750Val mutants. Further, Contact Order analysis indicated that the Aromatic–sulfur interactions were destabilizing in the mutants. Overall, these <em>in-silico</em> analysis has revealed a destabilizing mutations suggesting pathogenic variants in POLG1 gene.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101870"},"PeriodicalIF":4.4,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Involvement of mitochondria in Alzheimer’s disease pathogenesis and their potential as targets for phytotherapeutics","authors":"Swathi Maruthiyodan , Kamalesh Dattaram Mumbrekar , Kanive Parashiva Guruprasad","doi":"10.1016/j.mito.2024.101868","DOIUrl":"10.1016/j.mito.2024.101868","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is the leading cause of dementia around the globe. The disease's genesis is multifaceted, and its pathophysiology is complicated. Malfunction of mitochondria has been regarded as one of the intracellular events that are substantially damaged in the onset of AD and are likely a common trait of other neurodegenerative illnesses. Several mitochondrial characteristics begin to diminish with age, eventually reaching a state of significant functional failure concurrent with the beginning of neurodegenerative diseases, however, the exact timing of these processes is unknown. Mitochondrial malfunction has a multitude of negative repercussions, including reduced calcium buffering and secondary excitotoxicity contributing to synaptic dysfunction, also free radical production, and activation of the mitochondrial permeability transition. Hence mitochondria are considered a therapeutic target in neurodegenerative disorders such as Alzheimer's. Traditional medicinal systems practiced in different countries employing various medicinal plants postulated to have potential role in the therapy and management of memory impairment including amnesia, dementia as well as AD. Although, the preclinical and clinical studies using these medicinal plants or plant products have demonstrated the therapeutic efficacy for AD, the precise mechanism of action is still obscure. Therefore, this review discusses the contribution of mitochondria towards AD pathogenesis and considering phytotherapeutics as a potential therapeutic strategy.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101868"},"PeriodicalIF":4.4,"publicationDate":"2024-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1567724924000266/pdfft?md5=ee3428e08be57285789e5315f9884e44&pid=1-s2.0-S1567724924000266-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ancient mitogenomes suggest complex maternal history of one of the oldest settlements of western India","authors":"Bhavna Ahlawat , Lomous Kumar , Abhijit Ambekar , Jagmahender Singh Sehrawat , Yadubir Singh Rawat , Niraj Rai","doi":"10.1016/j.mito.2024.101871","DOIUrl":"10.1016/j.mito.2024.101871","url":null,"abstract":"<div><p>The ancient township of Vadnagar tells a story of a long chain of cultural diversity and exchange. Vadnagar has been continuously habituated and shows a presence of rich cultural amalgamation and continuous momentary sequences between the 2th century BCE and present-day. Seven cultural periods developed a complex and enriched settlement at Vadnagar in spatio-temporality. Although archaeological studies done on this oldest settlement suggested a rich cultural heritage, the genetic studies to pinpoint the genetic ancestry was lacking till date. In our current study we have for the first time reconstructed the complete mitogenomes of medieval individuals of the Vadnagar archaeological site in Gujarat. The study aimed to investigate the cosmopolitan nature of the present population as well as the migratory pattern and the inflow of different groups through trade, cultural and religious practices. Our analysis suggests heterogeneous nature of the medieval population of Vadnagar with presence of deeply rooted local ancestral components as well as central Asian genetic ancestry. This Central Asian component associated with mitochondrial haplotype U2e was not shared with any individual from India, but rather with individuals from the Bronze Age of Tajikistan and with an earlier age of coalescence. In summary, we propose that the medieval site of Vadnagar in western India was rich in cultural and genetic aspects, with both local and western Eurasian components.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101871"},"PeriodicalIF":4.4,"publicationDate":"2024-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification of a novel MT-ND3 variant and restoring mitochondrial function by allotopic expression of MT-ND3 gene","authors":"Nurun Nahar Borna , Yoshihito Kishita , Masaru Shimura , Kei Murayama , Akira Ohtake , Yasushi Okazaki","doi":"10.1016/j.mito.2024.101858","DOIUrl":"10.1016/j.mito.2024.101858","url":null,"abstract":"<div><p>Mitochondrial diseases are caused by nuclear, or mitochondrial DNA (mtDNA) variants and related co-factors. Here, we report a novel m.10197G > C variant in <em>MT-ND3</em> in a patient, and two other patients with m.10191 T > C. <em>MT-ND3</em> variants are known to cause Leigh syndrome or mitochondrial complex I deficiency. We performed the functional analyses of the novel m.10197G > C variant that significantly lowered MT-ND3 protein levels, causing complex I assembly and activity deficiency, and reduction of ATP synthesis. We adapted a previously described re-engineering technique of delivering mitochondrial genes into mitochondria through codon optimization for nuclear expression and translation by cytoplasmic ribosomes to rescue defects arising from the <em>MT-ND3</em> variants. We constructed mitochondrial targeting sequences along with the codon-optimized <em>MT-ND3</em> and imported them into the mitochondria. To achieve the goal, we imported codon-optimized <em>MT-ND3</em> into mitochondria in three patients with m.10197G > C and m.10191 T > C missense variants in the <em>MT-ND3</em>. Nuclear expression of the <em>MT-ND3</em> gene partially restored protein levels, complex I deficiency, and significant improvement of ATP production indicating a functional rescue of the mutant phenotype. The codon-optimized nuclear expression of mitochondrial protein and import inside the mitochondria can supplement the requirements for ATP in energy-deficient mitochondrial disease patients.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101858"},"PeriodicalIF":4.4,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140028423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-03-01DOI: 10.1016/j.mito.2024.101850
Kristina Xiao Liang
{"title":"Interplay of mitochondria and diabetes: Unveiling novel therapeutic strategies","authors":"Kristina Xiao Liang","doi":"10.1016/j.mito.2024.101850","DOIUrl":"10.1016/j.mito.2024.101850","url":null,"abstract":"<div><p>The interplay between mitochondrial function and diabetes has gained significant attention due to its crucial role in the pathogenesis and progression of the disease. Mitochondria, known as the cellular powerhouses, are essential for glucose metabolism. Dysfunction of these organelles has been implicated in the development of insulin resistance and beta-cell failure, both prominent features of diabetes. This comprehensive review explores the intricate mechanisms involved, including the generation of reactive oxygen species and the impact of mitochondrial DNA (mtDNA) mutations. Moreover, the review delves into emerging therapeutic strategies that specifically target mitochondria, such as mitochondria-targeted antioxidants, agents promoting mitochondrial biogenesis, and compounds modulating mitochondrial dynamics. The potential of these novel approaches is critically evaluated, taking into account their benefits and limitations, to provide a well-rounded perspective. Ultimately, this review emphasizes the importance of advancing our understanding of mitochondrial biology to revolutionize the treatment of diabetes.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"75 ","pages":"Article 101850"},"PeriodicalIF":4.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1567724924000084/pdfft?md5=1591569e1912e9b9ef8c3caa0c55618d&pid=1-s2.0-S1567724924000084-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139707136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
MitochondrionPub Date : 2024-02-28DOI: 10.1016/j.mito.2024.101853
B. Disha , Rohan Peter Mathew , Ashwin B. Dalal , Ajay K. Mahato , Kapaettu Satyamoorthy , Keshav K. Singh , Kumarasamy Thangaraj , Periyasamy Govindaraj
{"title":"Mitochondria in biology and medicine – 2023","authors":"B. Disha , Rohan Peter Mathew , Ashwin B. Dalal , Ajay K. Mahato , Kapaettu Satyamoorthy , Keshav K. Singh , Kumarasamy Thangaraj , Periyasamy Govindaraj","doi":"10.1016/j.mito.2024.101853","DOIUrl":"10.1016/j.mito.2024.101853","url":null,"abstract":"<div><p>Mitochondria are an indispensable part of the cell that plays a crucial role in regulating various signaling pathways, energy metabolism, cell differentiation, proliferation, and cell death. Since mitochondria have their own genetic material, they differ from their nuclear counterparts, and dysregulation is responsible for a broad spectrum of diseases. Mitochondrial dysfunction is associated with several disorders, including neuro-muscular disorders, cancer, and premature aging, among others. The intricacy of the field is due to the cross-talk between nuclear and mitochondrial genes, which has also improved our knowledge of mitochondrial functions and their pathogenesis. Therefore, interdisciplinary research and communication are crucial for mitochondrial biology and medicine due to the challenges they pose for diagnosis and treatment. The ninth annual conference of the Society for Mitochondria Research and Medicine (SMRM)- India, titled “Mitochondria in Biology and Medicine” was organized at the Centre for DNA Fingerprinting and Diagnostics (CDFD), Hyderabad, India, on June 21–23, 2023. The latest advancements in the field of mitochondrial biology and medicine were discussed at the conference. In this article, we summarize the entire event for the benefit of researchers working in the field of mitochondrial biology and medicine.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"76 ","pages":"Article 101853"},"PeriodicalIF":4.4,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}