ReviewGeroScience2021
Mitochondrial-derived peptides in aging and age-related diseases.
Review in GeroScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Peptide Regulation of Gene Expression: A Systematic Review.Molecules (Basel, Switzerland) · 2021Pooled it
- LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection.Redox biology · 2026Article
- The selenium-enrichedFrontiers in microbiology · 2026Article
- Mitochondrial-Derived Peptides as Therapeutics and Biomarkers for Combating Vascular Aging and Associated Cardiovascular Diseases.Current cardiology reviews · 2026Review
- MOTS‑c protects against placental injury via Nrf2 activation in hypoxia‑induced intrauterine growth restriction mice.International journal of molecular medicine · 2026Article
- Exercise attenuates the hallmarks of aging: Novel perspectives.Journal of sport and health science · 2025Review
- Age-diet interactions significantly influence intratumoral gene expression, gut microbiome signature and tumor microenvironment in colorectal cancer.Neoplasia (New York, N.Y.) · 2025Article
- Insights into the Biomarker Potential of Humanin and Mots-c Expression and Telomere Length in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- MOTS-C levels ın ındividuals with and without obesity and ıts association with ınflammation, insulin resistance and endothelial dysfunction.Archives of endocrinology and metabolism · 2025Article
- Biological and translational attributes of mitochondrial DNA copy number: Laboratory perspective to clinical relevance.World journal of methodology · 2025Review
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Mitochondria‑derived peptides: Promising microproteins in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Inter- and intracellular mitochondrial communication: signaling hubs in aging and age-related diseases.Cellular & molecular biology letters · 2024Review
- Article
- Expression Patterns of MOTS-c in Adrenal Tumors: Results from a Preliminary Study.International journal of molecular sciences · 2024Article
- The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism.Antioxidants (Basel, Switzerland) · 2024Article
- MOTS-c is an effective target for treating cancer-induced bone pain through the induction of AMPK-mediated mitochondrial biogenesis.Acta biochimica et biophysica Sinica · 2024Article
- Physical Activity and Oxidative Stress in Aging.Antioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.American journal of physiology. Endocrinology and metabolism · 2024Article
- Mitochondrial Targeted Interventions for Aging.Cold Spring Harbor perspectives in medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in the levels of mitochondrial-derived peptides contributes to aging and age-related diseases. In particular, we discuss how mitochondrial-derived peptides, humanin and MOTS-c, contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and cognitive decline. Genetic variations in the coding region of humanin and MOTS-c that are associated with age-related diseases are also reviewed, with particular emphasis placed on how mitochondrial variants might, in turn, regulate MDP expression and age-related phenotypes. Taken together, these observations suggest that mitochondrial-derived peptides influence or regulate a number of key aspects of aging and that strategies directed at increasing mitochondrial-derived peptide levels might have broad beneficial effects.
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.