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Mots-C

Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1, Mitochondrial-derived peptide MOTS-c

Quick Stats
Studies 137
Trials 5
Score 2
2025 pubmed 1 citations

Circulating mitochondrial biomarkers in acute coronary syndrome.

Iboleon-Jimenez. Andrea A; Sánchez-Quintero. María J MJ; Carmona-Segovia. Ada D M ADM; Sojo. Bélen B; Fernández-Ramos. Ana María AM; García-Rodríguez. Luis L; Molina-Ramos. Ana I AI; García-Pinilla. José Manuel JM; Jimenez-Navarro. Manuel M; Ortega-Gomez. Almudena A

Key Findings

  • Acute coronary syndrome (heart attack) significantly reduces plasma MOTS‑c and PGC‑1α levels.
  • MOTS‑c levels positively correlate with troponin (a heart‑damage marker) and hemoglobin.
  • PGC‑1α levels are negatively correlated with glucose and positively correlated with HDL‑cholesterol; no sex differences were observed for either marker.

Practical Outcomes

  • For biohackers, the main takeaway is that MOTS‑c may serve as a blood biomarker of heart stress, but the study does not provide guidance on dosing or supplementation. While it hints that boosting MOTS‑c could be beneficial, there is no direct evidence yet, so any intervention would be speculative and should await further clinical trials.

Summary

People having a heart attack have lower levels of the mitochondrial peptide MOTS‑c (and the protein PGC‑1α) in their blood. The study found no difference between men and women, and it linked MOTS‑c levels to heart‑damage markers like troponin and to blood‑cell counts. These findings suggest MOTS‑c could be a useful signal of heart stress, but the research does not test any treatments.

Abstract

Acute coronary syndrome (ACS) is the leading cause of mortality in developed countries. Mitochondrial dysfunction is a hallmark of various cardiometabolic diseases, including ACS. Emerging evidence suggests that evaluating mitochondrial biomarkers in plasma may offer valuable insights into the pathophysiology and management of these conditions. The present study aims to analyse the effect of ACS, sex and their interaction on plasma levels of mitochondrial markers, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) and citrate syntetase (CS). A total of 18 ACS patients (8 women and 10 men) and 20 controls (8 women and 12 men) were included in this study. Venous blood samples were collected from participants after a 12-h overnight fast. Plasma levels of mitochondrial PGC-1α, MOTS-c and CS were measured. ACS significantly reduced plasma levels of PGC-1α and MOTS-c. Sex did not shown a significant effect on these markers. Additionally, MOTS-c positively correlated with the first troponin and hemoglobin, PGC-1α negatively correlated with glucose and positively with HDL-cholesterol, and CS showed negative correlations with NT-proBNP, C-reactive protein, and hemoglobin. Mitochondria markers, MOTS-c and PGC-1α, are altered in ACS patients, with no observed sex differences. These findings represent an initial step toward integrating personalized medicine into the clinical management of ACS. Nonetheless, further studies are required to fully elucidate the role of these markers in this pathology.

Study Information

Provider

pubmed

Year

2025

Date

2025-05-15T00:00:00.000Z

DOI

10.3389/fmed.2025.1568305

Citations

1

References

33