Abstract
Cardiovascular diseases, including coronary artery disease, ischemic heart diseases such as acute myocardial infarction and postischemic heart failure, heart failure of other etiologies, and cardiac arrhythmias, belong to the leading causes of death. Activation of capsaicin-sensitive sensory nerves by the transient receptor potential vanilloid 1 (TRPV1) capsaicin receptor and other receptors, as well as neuropeptide mediators released from them upon stimulation, play important physiological regulatory roles. Capsaicin-sensitive sensory nerves also contribute to the development and progression of some cardiac diseases, as well as to mechanisms of endogenous stress adaptation leading to cardioprotection. In this review, we summarize the role of capsaicin-sensitive afferents and the TRPV1 ion channel in physiological and pathophysiological functions of the heart based mainly on experimental results and show their diagnostic or therapeutic potentials. Although the actions of several other channels or receptors expressed on cardiac sensory afferents and the effects of TRPV1 channel activation on different non-neural cell types in the heart are not precisely known, most data suggest that stimulation of the TRPV1-expressing sensory nerves or stimulation/overexpression of TRPV1 channels have beneficial effects in cardiac diseases.
Highlights
Introduction and BackgroundCapsaicin is the active, pungent component of chili peppers that is able to selectively activate and, after high dose administration, selectively defunctionalize an important subpopulation of sensory neurons with thinly myelinated Aδ or unmyelinated C fibers [1]
Capsaicin repressed reactive oxygen species (ROS) generation and caspase-3 activation in Human umbilical vein endothelial cells (HUVECs) cells pretreated with oxidized low-density lipoprotein, protected macrophage RAW 264.7 cells against foam cell formation, and induced autophagy through AMP-activated protein kinase signaling pathway in oxLDL-treated vascular smooth muscle cells (VSMCs), which suggests a protective role of transient receptor potential vanilloid 1 (TRPV1) activation against oxLDL-induced vascular dysfunctions [66,67]
This review summarizes the data about the role of the cardiac capsaicin-sensitive sensory nerves and the TRPV1 receptor in cardiac pathologies, including coronary heart disease, myocardial infarction, heart failure, and arrhythmias
Summary
Pungent component of chili peppers (characterized by Scoville Heat Units, SHU, 15–16 million SHU for pure capsaicin) that is able to selectively activate and, after high dose administration, selectively defunctionalize an important subpopulation of sensory neurons with thinly myelinated Aδ or unmyelinated C fibers [1]. Experimental and clinical studies have identified an essential role of cardiac sensory nerves, including the capsaicin-sensitive fibers in cardiac physiology and pathologies. TRPV1 receptors expressed both on these sensory nerves and on other non-neuronal cells, as well as the mediators (mainly sensory neuropeptides) released upon their activation, play important regulatory roles in the development and/or progression of cardiovascular diseases [11]. Despite intensive investigation in this field, data are still not coherent regarding the modulatory effects of TRPV1 and capsaicin-sensitive sensory nerves on cardiac pathologies. In this review, we summarized data on the role of capsaicin-sensitive nerves and TRPV1 channels in cardiac physiology and pathologies and summarized their diagnostic or therapeutic potential. Available data in the literature so far are mainly obtained from preclinical experiments, since only a very limited number of clinical investigations have been performed in this field
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