ArticleThe Journal of biological chemistry2015
Accumulation of Mitochondrial DNA Mutations Disrupts Cardiac Progenitor Cell Function and Reduces Survival.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Pathogenic Role of mTOR Signaling in Cardiometabolic Disease: Implications for Heart, Liver, and Kidney Dysfunction.Physiological research · 2025Review
- Hippocampal mitophagy contributes to spatial memory via maintaining neurogenesis during the development of mice.CNS neuroscience & therapeutics · 2024Article
- Endoplasmic reticulum stress and alterations of peroxiredoxins in aged hearts.Mechanisms of ageing and development · 2023Article
- The Calcineurin-Drp1-Mediated Mitochondrial Fragmentation Is Aligned with the Differentiation of c-Kit Cardiac Progenitor Cells.International journal of stem cells · 2023Article
- Deciphering functional roles and interplay between Beclin1 and Beclin2 in autophagosome formation and mitophagy.Science signaling · 2023Article
- Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis.International journal of molecular sciences · 2021Review
- Mitochondrial and Autophagic Regulation of Adult Neurogenesis in the Healthy and Diseased Brain.International journal of molecular sciences · 2021Review
- Mitochondria and autophagy in adult stem cells: proliferate or differentiate.Journal of muscle research and cell motility · 2020Article
- Review
- Aging is associated with a decline in Atg9b-mediated autophagosome formation and appearance of enlarged mitochondria in the heart.Aging cell · 2020Article
- Nuclear Parkin Activates the ERRα Transcriptional Program and Drives Widespread Changes in Gene Expression Following Hypoxia.Scientific reports · 2020Article
- Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis.Journal of clinical medicine · 2020Review
- BNIP3L/NIX and FUNDC1-mediated mitophagy is required for mitochondrial network remodeling during cardiac progenitor cell differentiation.Autophagy · 2019Article
- Evolving and Expanding the Roles of Mitophagy as a Homeostatic and Pathogenic Process.Physiological reviews · 2019Review
- Review
- Mitochondrial diseases caused by mtDNA mutations: a mini-review.Therapeutics and clinical risk management · 2018Review
- Decline in cellular function of aged mouse c-kitThe Journal of physiology · 2017Article
- Eat, breathe, ROS: controlling stem cell fate through metabolism.Expert review of cardiovascular therapy · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
Transfer of cardiac progenitor cells (CPCs) improves cardiac function in heart failure patients. However, CPC function is reduced with age, limiting their regenerative potential. Aging is associated with numerous changes in cells including accumulation of mitochondrial DNA (mtDNA) mutations, but it is unknown how this impacts CPC function. Here, we demonstrate that acquisition of mtDNA mutations disrupts mitochondrial function, enhances mitophagy, and reduces the replicative and regenerative capacities of the CPCs. We show that activation of differentiation in CPCs is associated with expansion of the mitochondrial network and increased mitochondrial oxidative phosphorylation. Interestingly, mutant CPCs are deficient in mitochondrial respiration and rely on glycolysis for energy. In response to differentiation, these cells fail to activate mitochondrial respiration. This inability to meet the increased energy demand leads to activation of cell death. These findings demonstrate the consequences of accumulating mtDNA mutations and the importance of mtDNA integrity in CPC homeostasis and regenerative potential.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.