ArticleMolecular and cellular biochemistry2017
Angiotensin (1-7) facilitates cardioprotection of ischemic preconditioning on ischemia-reperfusion-challenged rat heart.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- A novel angiotensin(1-7) agonist, PNA5, reduces ischemic reperfusion injury and cardiac dysfunction.Frontiers in cardiovascular medicine · 2026Article
- Angiotensin-(1-9) Improves the Cardioprotective Effects of Del Nido Cardioplegia Against Ischemia/Reperfusion Injury.Journal of cellular and molecular medicine · 2025Article
- Novel Molecules Targeting Metabolism and Mitochondrial Function in Cardiac Diseases.Current cardiology reviews · 2025Review
- Chrysin restores the cardioprotective effect of ischemic preconditioning in diabetes-challenged rat heart.Heliyon · 2023Article
- Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases.Cell cycle (Georgetown, Tex.) · 2023Review
- Modulation ofJournal of pharmacopuncture · 2022Article
- Cardioprotective Mechanisms against Reperfusion Injury in Acute Myocardial Infarction: Targeting Angiotensin II Receptors.Biomedicines · 2022Review
- Alamandine alleviated heart failure and fibrosis in myocardial infarction mice.Biology direct · 2022Article
- Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning.International journal of molecular sciences · 2022Review
- An inquest into regulatory mechanism of caveolin by ischemic preconditioning against orchidectomy-challenged rat heart.Molecular and cellular biochemistry · 2021Article
- Mechanism of the hypoxia inducible factor 1/hypoxic response element pathway in rat myocardial ischemia/diazoxide post‑conditioning.Molecular medicine reports · 2020Article
- Antioxidant Solution in Combination with Angiotensin-(1-7) Provides Myocardial Protection in Langendorff-Perfused Rat Hearts.Oxidative medicine and cellular longevity · 2020Article
- Investigation of antioxidative effects of a cardioprotective solution in heart tissue.Molecular and cellular biochemistry · 2019Article
- The Renin-Angiotensin-Aldosterone System as a Therapeutic Target in Late Injury Caused by Ischemia-Reperfusion.International journal of endocrinology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic preconditioning (IPC) is one of the most promising strategies used to protect the myocardium from ischemia-reperfusion injury. Ang (1-7) exhibits cardioprotective activity; however, its therapeutic potential on IPC-induced cardioprotection has not been reported in ischemia-reperfusion injury till date. Therefore, the first set of experiment was designed to evaluate the direct effect of Ang (1-7), in perfusion medium, on cardioprotective activity of IPC in rat heart challenged to ischemia-reperfusion injury. In addition, the acute and chronic effects of pretreated Ang (1-7) were investigated on cardioprotection of IPC in ischemia-reperfusion-challenged hearts in subsequent sets of experiments. The results showed that Ang (1-7) potentiated the IPC-induced increase in coronary flow and heart rate, decrease in lactate dehydrogenase and creatine kinase activity, ventricular fibrillation, and infarct size in ischemia-reperfusion-challenged animals in direct and chronic sets of experiments. Further, Ang (1-7) enhanced the IPC-induced attenuation in mitochondrial dysfunction, oxidative stress, and apoptosis in ischemia-reperfusion-challenged hearts in both sets of experiments. A-779, Mas receptor antagonist, abrogated potentiation effects of Ang (1-7) on IPC-induced cardioprotection in ischemia-reperfusion-challenged rats in the above set of experiments. These observations indicate that Ang (1-7)/Mas receptor activation could be a potential adjuvant to IPC during ischemia-reperfusion-induced cardiac injury.
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