Physiological and Pathological Role of TRPV1, TRPV2 and TRPV4 Channels in Heart

被引:20
作者
Gorbunov, Alexandr S. [1 ]
Maslov, Leonid N. [1 ]
Jaggi, Amteshwar S. [2 ]
Singh, Nirmal [2 ]
De Petrocellis, Luciano [3 ]
Boshchenko, Alla A. [1 ]
Roohbakhsh, Ali [4 ]
Bezuglov, Vladimir V. [5 ]
Oeltgen, Peter R. [6 ]
机构
[1] Russian Acad Sci, Cardiol Res Inst, Lab Expt Cardiol, Tomsk Natl Res Med Ctr, Kyevskaya 111A, Tomsk 634012, Russia
[2] Punjabi Univ, Dept Pharmaceut Sci & Drug Res, Patiala, Punjab, India
[3] CNR, Ist Chim Biomol, Pozzuoli, NA, Italy
[4] Mashhad Univ Med Sci, Pharmaceut Res Ctr, Sch Pharm, Dept Pharmacodynam & Toxicol, Mashhad, Razavi Khorasan, Iran
[5] RAS, Acad MM Shemyakin & Yu A Ovchinnikova, Inst Bioorgan Chem, Moscow, Russia
[6] Univ Kentucky, Coll Med, Dept Pathol, Lexington, KY USA
基金
俄罗斯科学基金会;
关键词
Heart; TRPV1; TRPV2; TRPV4; cardiomyocytes; cardiomyopathy; GENE-RELATED PEPTIDE; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; VANILLOID RECEPTOR VR1; CAPSAICIN-RECEPTOR; COMPETITIVE ANTAGONIST; POSTISCHEMIC RECOVERY; REPERFUSION INJURY; ACTIVATION; RAT; CANNABIDIOL;
D O I
10.2174/1573403X15666190307112326
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Transient receptor potential vanilloid channel 2 (TRPV2) is required for normal cardiac contractility. The stimulation of TRPV1 in isolated cardiomyocytes can aggravate the effect of hypoxia/reoxygenation (H/R) on H9C2 cells. The knockout of the TRPV1 gene promotes increased tolerance of the isolated perfused heart to the impact of ischemia/reperfusion (I/R). However, activation of TRPV1 increases the resistance of the heart to I/R due to calcitonin gene-related peptide (CGRP) release from afferent nerve endings. It has been established that TRPV1 and TRPV2 are involved in the pathogenesis of myocardial infarction and, in all likelihood, ensure the cardiac tolerance to the ischemia/reperfusion. It has also been documented that the activation of TRPV4 negatively affects the stability of cardiomyocytes to the H/R. The blockade of TRPV4 can be considered as a new approach to the prevention of I/R injury of the heart. Studies also indicate that TRPV1 is involved in the pathogenesis of cardiac hypertrophy and that TRPV2 channels participate in the pathogenesis of dilated cardiomyopathy. Excessive expression of TRPV2 leads to chronic Ca2+-overload of cardiomyocytes, which may contribute to the development of cardiomyopathy.
引用
收藏
页码:244 / 251
页数:8
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