Semaglutide enhances PINK1/Parkin‑dependent mitophagy in hypoxia/reoxygenation‑induced cardiomyocyte injury DOI Creative Commons
Liqin Li,

Lili Jin,

Yaping Tian

et al.

Molecular Medicine Reports, Journal Year: 2025, Volume and Issue: 31(5), P. 1 - 12

Published: Feb. 25, 2025

The present study aimed to explore how semaglutide can help protect the heart from injury caused by hypoxia/reoxygenation (H/R) and reveal underlying mechanism. Briefly, AC16 cardiomyocytes were subjected 8 h of hypoxia followed 12 reoxygenation simulate H/R. cells divided into following five groups: Normoxia, H/R, H/R + semaglutide, rapamycin (autophagy inducer), 3‑methyladenine (3‑MA; autophagy inhibitor) groups. Cell viability was examined using a Counting Kit‑8 assay, ATP levels bioluminescent detection kit, reactive oxygen species (ROS) production detected ROS Assay Kit, monomeric red fluorescent protein (mRFP)‑green (GFP)‑LC3 assessed tandem mRFP‑GFP fluorescence microscopy, while autophagosomes observed transmission electron microscopy. Furthermore, expression markers (LC3, p62 Beclin1) regulators mitochondrial [PTEN‑induced putative kinase protein‑1 (PINK1) Parkin] western blot analysis. In cells, exposure led an increase in oxidative stress. This condition also induced activity, as evidenced number autophagosomes, elevated LC3‑II/LC3‑I ratio, upregulation p62, Beclin1, PINK1 Parkin compared with those cultured under normoxia. Notably, treatment or effectively reversed H/R‑induced stress, enhanced changes autophagosome LC3BII/LC3BI increased PINK1, expression. use 3‑MA exhibited distinct effects same conditions; it exacerbated decreased activity reduced ratio. conclusion, found reduce stress via ROS/PINK1/Parkin/p62 pathway. offers novel understanding may heart, suggests its potential myocardial ischemia/reperfusion injury.

Language: Английский

Semaglutide enhances PINK1/Parkin‑dependent mitophagy in hypoxia/reoxygenation‑induced cardiomyocyte injury DOI Creative Commons
Liqin Li,

Lili Jin,

Yaping Tian

et al.

Molecular Medicine Reports, Journal Year: 2025, Volume and Issue: 31(5), P. 1 - 12

Published: Feb. 25, 2025

The present study aimed to explore how semaglutide can help protect the heart from injury caused by hypoxia/reoxygenation (H/R) and reveal underlying mechanism. Briefly, AC16 cardiomyocytes were subjected 8 h of hypoxia followed 12 reoxygenation simulate H/R. cells divided into following five groups: Normoxia, H/R, H/R + semaglutide, rapamycin (autophagy inducer), 3‑methyladenine (3‑MA; autophagy inhibitor) groups. Cell viability was examined using a Counting Kit‑8 assay, ATP levels bioluminescent detection kit, reactive oxygen species (ROS) production detected ROS Assay Kit, monomeric red fluorescent protein (mRFP)‑green (GFP)‑LC3 assessed tandem mRFP‑GFP fluorescence microscopy, while autophagosomes observed transmission electron microscopy. Furthermore, expression markers (LC3, p62 Beclin1) regulators mitochondrial [PTEN‑induced putative kinase protein‑1 (PINK1) Parkin] western blot analysis. In cells, exposure led an increase in oxidative stress. This condition also induced activity, as evidenced number autophagosomes, elevated LC3‑II/LC3‑I ratio, upregulation p62, Beclin1, PINK1 Parkin compared with those cultured under normoxia. Notably, treatment or effectively reversed H/R‑induced stress, enhanced changes autophagosome LC3BII/LC3BI increased PINK1, expression. use 3‑MA exhibited distinct effects same conditions; it exacerbated decreased activity reduced ratio. conclusion, found reduce stress via ROS/PINK1/Parkin/p62 pathway. offers novel understanding may heart, suggests its potential myocardial ischemia/reperfusion injury.

Language: Английский

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