Telmisartan protects against microvascular dysfunction during myocardial ischemia/reperfusion injury by activation of peroxisome proliferator-activated receptor γ
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Published on: January 10, 2025
Xiao-Cong Zeng1, Xing-San Li, Hong Wen
1Department of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, People's Republic of China.
Background:
We investigated the potential of telmisartan to improve microvascular dysfunction induced by myocardial ischemia/reperfusion (I/R) injury by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway.
Methods:
Forty-eight male rabbits were randomly allocated into sham-operated, I/R, GW9662, telmisartan, telmisartan-GW9662, or candesartan groups. Rabbits were anesthetized, and the left anterior descending coronary artery (LAD) was ligated for 60 minutes. Following reperfusion for 6 hours, angiotensin II content of the heart was determined using radioimmunoassay. Myocardial neutrophil accumulation and microvessel cross-sectional area were examined histologically. Myocardial capillaries were examined with transmission electron microscopy. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the myocardium were measured using enzyme-linked immunosorbent assay. Western blot was utilized for investigating the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and PPARG.
Results:
Angiotensin II concentration was significantly increased in all treatment groups compared with the sham-operated group (P < 0.05, all). Accumulation of polymorphonuclear neutrophils was significantly lower, while microvessel cross-sectional area was significantly higher in the telmisartan, telmisartan-GW9662, and candesartan groups compared with the I/R group (P < 0.05). ICAM-1 and VCAM-1 levels were also significantly lower, and correlated with lower NF-κB expression in these groups. The effects were the most significant in the telmisartan group compared with the telmisartan-GW9662 and candesartan groups. Telmisartan significantly increased PPARG protein expression compared with all other groups (P < 0.05, all).
Conclusions:
Except for the typical effects of angiotensin II-receptor blocker, telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway.
Insights
Telmisartan treatment improved microvascular dysfunction following myocardial ischemia/reperfusion (I/R) injury. This effect was mediated by activating the peroxisome proliferator-activated receptor gamma (PPARG) pathway, independent of its angiotensin II-receptor blocking action.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cellular Biology
Background:
- Myocardial ischemia/reperfusion (I/R) injury causes microvascular dysfunction.
- Peroxisome proliferator-activated receptor gamma (PPARG) is a potential therapeutic target.
Purpose of the Study:
- To investigate telmisartan's potential to improve microvascular dysfunction in myocardial I/R injury.
- To determine if PPARG pathway activation mediates telmisartan's effects.
Main Methods:
- A rabbit model of myocardial I/R injury was used.
- Animals were treated with telmisartan, candesartan, or a PPARG inhibitor (GW9662).
- Evaluated myocardial angiotensin II, neutrophil accumulation, microvessel area, ICAM-1, VCAM-1, NF-κB, and PPARG expression.
Main Results:
- Telmisartan significantly improved microvascular function, reducing neutrophil accumulation and increasing microvessel area.
- Telmisartan decreased ICAM-1, VCAM-1, and NF-κB levels.
- Telmisartan markedly upregulated PPARG protein expression compared to other groups.
Conclusions:
- Telmisartan ameliorates microvascular dysfunction in myocardial I/R injury.
- PPARG pathway activation is a key mechanism underlying telmisartan's beneficial effects.
- Telmisartan offers therapeutic potential beyond its angiotensin II-receptor blocking activity.
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