ArticleCell reports2021
Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.
Article in Cell reports, 2021. 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 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- The identity crisis of cryptic lncRNAs: when non-coding RNAs translate into small peptides.The EMBO journal · 2026Review
- Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.Inflammation and regeneration · 2026Article
- MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases.Journal of translational medicine · 2026Review
- Reduced Circulating MOTS-c Levels in Hashimoto's Thyroiditis Reflect Integrated Autoimmune and Metabolic Dysregulation: A Cross-Sectional Study.Journal of clinical medicine · 2026Article
- Are serum MOTS-c levels and MOTS-c m.1382A>C polymorphism related to polycystic ovary syndrome?Archives of endocrinology and metabolism · 2026Article
- Mitochondrial-derived microproteins in lung disease: insights and implications.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- SLC25A3 promotes hepatocellular carcinoma progression by inducing mitochondrial dysfunction and chromatin remodeling.Translational cancer research · 2025Article
- Microproteins in Metabolic Biology: Emerging Functions and Potential Roles as Nutrient-Linked Biomarkers.International journal of molecular sciences · 2025Review
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Microproteins in Metabolism.Cells · 2025Review
- MOTS-c modulates pancreatic islet function in rats and pigs in vitro.Histochemistry and cell biology · 2025Article
- MOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration.Materials today. Bio · 2025Article
- Could MOTS-c Levels in Children with Type 1 Diabetes Mellitus Be an Indicator for Early Diabetic Kidney Disease?Journal of clinical research in pediatric endocrinology · 2025Article
- Targeting CD4+ T Cell Glucose Metabolism: A Novel Immunotherapeutic Approach for Type 1 Diabetes.Biomolecules · 2025Review
- Mitochondrial Dysfunction in the Development and Progression of Cardiometabolic Diseases: A Narrative Review.Journal of clinical medicine · 2025Review
- Endogenous micropeptides as potential diagnostic biomarkers and therapeutic drugs.Frontiers in pharmacology · 2025Review
- Mitochondrial-derived peptides in cardiovascular disease: Novel insights and therapeutic opportunities.Journal of advanced research · 2024Review
- The correlation between mitochondrial derived peptide (MDP) and metabolic states: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2024Review
- Expression Patterns of MOTS-c in Adrenal Tumors: Results from a Preliminary Study.International journal of molecular sciences · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are principal metabolic organelles that are increasingly unveiled as immune regulators. However, it is currently not known whether mitochondrial-encoded peptides modulate T cells to induce changes in phenotype and function. In this study, we found that MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) prevented autoimmune β cell destruction by targeting T cells in non-obese diabetic (NOD) mice. MOTS-c ameliorated the development of hyperglycemia and reduced islet-infiltrating immune cells. Furthermore, adoptive transfer of T cells from MOTS-c-treated NOD mice significantly decreased the incidence of diabetes in NOD-severe combined immunodeficiency (SCID) mice. Metabolic and genomic analyses revealed that MOTS-c modulated T cell phenotype and function by regulating T cell receptor (TCR)/mTOR complex 1 (mTORC1) signaling. Type 1 diabetes (T1D) patients had a lower serum MOTS-c level than did healthy controls. Furthermore, MOTS-c reduced T cell activation by alleviating T cells from the glycolytic stress in T1D patients, suggesting therapeutic potential. Our findings indicate that MOTS-c regulates the T cell phenotype and suppresses autoimmune diabetes.
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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 Socratic graph.