ArticleBMC cardiovascular disorders2013
Telmisartan protects against microvascular dysfunction during myocardial ischemia/reperfusion injury by activation of peroxisome proliferator-activated receptor γ.
Article in BMC cardiovascular disorders, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Nanocarrier-Based Therapeutic Strategies in Myocardial Ischemia-Reperfusion Injury: A Systematic Review of Preclinical Evidence.Biomedicines · 2026Review
- Platelets as Central Modulators of Post-Cardiac Arrest Syndrome: Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Single-Cell Transcriptomics of Human Acute Myocardial Infarction Reveals Oxidative Stress-Associated Cardiomyocyte Subpopulations and Candidate Predictive Signatures.Antioxidants (Basel, Switzerland) · 2025Article
- Article
- Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation.Journal of molecular and cellular cardiology plus · 2025Review
- Pharmacological Utility of PPAR Modulation for Angiogenesis in Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Roles of Peroxisome Proliferator-Activated Receptor Gamma on Brain and Peripheral Inflammation.Cellular and molecular neurobiology · 2018Review
- Long non-coding RNA-ROR aggravates myocardial ischemia/reperfusion injury.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma.Frontiers in pharmacology · 2017Article
- Telmisartan improves cardiac fibrosis in diabetes through peroxisome proliferator activated receptor δ (PPARδ): from bedside to bench.Cardiovascular diabetology · 2016Article
- MicroRNA-128 inhibition attenuates myocardial ischemia/reperfusion injury-induced cardiomyocyte apoptosis by the targeted activation of peroxisome proliferator-activated receptor gamma.Molecular medicine reports · 2016Article
- Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe 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.
methodsForty-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.
resultsAngiotensin 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).
conclusionsExcept for the typical effects of angiotensin II-receptor blocker, telmisartan improved microvascular dysfunction during myocardial I/R injury via the PPARG pathway.
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