MOTS-c · research summary
Frontiers in endocrinology · 2026. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.
Animal study investigating the effects of aerobic exercise and MOTS-c on diabetic myocardial fibrosis using transcriptomic profiling.
“This study delved into the molecular mechanisms behind how exercise and MOTS-c influence cardiac fibrosis in diabetes.”
Sprague-Dawley rats with induced type 2 diabetes.
“Sixty 8-week-old Sprague-Dawley rats, weighing in at 180 to 200 grams, were sourced from the reputable Chengdu Dashuo Experimental Animal Technology Co., Ltd. in Chengdu, China, and they were confirmed to be SPF-grade.”
60 rats divided into five groups of 10 each.
“Rats were randomly divided into 5 groups: (1) control group (C, n = 10), (2) diabetes group (D, n = 10), (3) outcomes of exercise on diabetic rats (DE, n = 10), (4) diabetic rats receiving MOTS-c (DM, n = 10), (5) combining exercise and MOTS-c (DME, n = 10).”
8 weeks of intervention following diabetes induction.
“The study aimed to assess the effects of different eight-week treatments on diabetes-induced cardiac fibrosis.”
Aerobic exercise and MOTS-c improved glucose and lipid metabolism, reduced collagen buildup, and improved systolic and diastolic heart functions in diabetic rats.
“Both approaches led to marked enhancements in glucose and lipid metabolism, lowered collagen buildup, and bettered both systolic and diastolic heart functions.”
Transcriptomic profiling identified THBS1 as a pivotal gene, with reduced activity in the THBS1/TGF-β pathway verified at mRNA and protein stages.
“Through transcriptomic profiling, THBS1 emerged as a pivotal gene that was altered, with reduced activity in the THBS1/TGF-β pathway verified at mRNA and protein stages.”
Aerobic exercise and MOTS-c alleviated myocardial fibrosis in diabetes, likely by inhibiting the THBS1/TGF-β signaling pathway.
“In a nutshell, these insights indicate that aerobic exercise and MOTS-c alleviate myocardial fibrosis in diabetes, most likely by putting a damper on the THBS1/TGF-β signaling pathway.”
The study did not validate myocardial collagen expression or matrix metalloproteinase activity, lacked direct validation of THBS1 as an upstream key factor using agonists/inhibitors, and did not measure MOTS-c levels in serum or plasma.
“In our study, myocardial fibrosis was confirmed using Masson staining and protein analysis, but we did not validate myocardial collagen expression or matrix metalloproteinase activity. Moreover, the study lacked direct validation of THBS1 as an upstream key factor through THBS1 agonists and inhibitors. Another limitation of our study is the failure to measure MOTS-c levels in serum or plasma.”
Source: PubMed 41710402 · DOI 10.3389/fendo.2026.1732329 · all study summaries