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The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

The acute myocardial infarction (AMI) and sudden cardiac death (SCD), both associated with acute cardiac ischemia, are one of the leading causes of adult death in economically developed countries. The development of new approaches for the treatment and prevention of AMI and SCD remains the highest p...

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Detalles Bibliográficos
Autores principales: Naryzhnaya, Natalia V., Maslov, Leonid N., Derkachev, Ivan A., Ma, Huijie, Zhang, Yi, Prasad, N. Rajendra, Singh, Nirmal, Fu, Feng, Pei, Jianming, Sarybaev, Akpay, Sydykov, Akylbek
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Editorial Department of Journal of Biomedical Research 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387748/
https://www.ncbi.nlm.nih.gov/pubmed/37183617
http://dx.doi.org/10.7555/JBR.36.20220125
Descripción
Sumario:The acute myocardial infarction (AMI) and sudden cardiac death (SCD), both associated with acute cardiac ischemia, are one of the leading causes of adult death in economically developed countries. The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine. A study on the cardiovascular effects of chronic hypoxia (CH) may contribute to the development of these methods. Chronic hypoxia exerts both positive and adverse effects. The positive effects are the infarct-reducing, vasoprotective, and antiarrhythmic effects, which can lead to the improvement of cardiac contractility in reperfusion. The adverse effects are pulmonary hypertension and right ventricular hypertrophy. This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion. It is an in-depth analysis of the published data on the underlying mechanisms, which can lead to future development of the cardioprotective effect of CH. A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.