Related Experiment Video
Updated: Aug 14, 2026
05:58
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
Published on: April 18, 2025
Metformin Attenuates Sepsis-Induced Cardiomyopathy via Inhibition of Reverse Electron Transfer at Mitochondrial
Nannan He1,2, Wen Cao2, Yannian Luo3
1The First School of Clinical Medicine, Lanzhou University, Lanzhou 730000, China.
Biology
|August 13, 2026
Summary
Sepsis-induced cardiomyopathy involves mitochondrial damage from excessive ROS. Metformin protects the heart by inhibiting this process, offering a potential therapy for septic myocardial dysfunction.
Area of Science:
- Biochemistry
- Cardiology
- Molecular Biology
Background:
- Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis.
- The precise molecular mechanisms underlying SICM are not fully understood, limiting therapeutic development.
Purpose of the Study:
- To investigate the role of mitochondrial reactive oxygen species (mtROS) generated via reverse electron transfer (RET) at mitochondrial complex I in SICM.
- To evaluate the protective effects of metformin, a complex I inhibitor, against SICM.
Main Methods:
- Utilized lipopolysaccharide-stimulated H9C2 cardiomyocytes and cecal ligation and puncture-induced septic rat models.
- Assessed mitochondrial function, mtROS production, inflammatory responses, and apoptosis.
- Measured cardiac function, oxidative stress, and myocardial injury in septic rats treated with metformin.
Main Results:
- Sepsis induced elevated mitochondrial membrane potential, succinate accumulation, and increased NADH/NAD+ ratio, favoring RET-mediated mtROS generation.
- Metformin inhibited complex I and suppressed RET-mediated mtROS without affecting forward electron transport (FET)-ROS.
- Metformin treatment attenuated inflammation, apoptosis, preserved cardiac function, and reduced myocardial injury in septic rats.
Conclusions:
- RET at mitochondrial complex I is a key contributor to septic myocardial injury.
- Metformin demonstrates potential as a therapeutic agent for preventing and treating SICM by targeting RET-mediated mtROS production.
