The effects of iloprost and beta3 receptor agonist on TRPA1 and TRPC1 immunreactivity  in an experimental lower extremty ischemia-reperfusion injury model

Üstünel, Latif; Özgüler, İbrahim Murat

doi:10.3906/sag-2104-68

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…There is evidence of a wide involvement of TRP channels in the pathogenesis of CVD caused by hypoxia and oxidative stress, as well as ischemia-reperfusion (I/R) [90,104,[112][113][114].…”

Section: Ion Channels With Transient Receptor Potential (Trpc Trpm7 T...mentioning

confidence: 99%

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Shemarova

2023

IJMS

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Chronic heart diseases, such as coronary heart disease, heart failure, secondary arterial hypertension, and dilated and hypertrophic cardiomyopathies, are widespread and have a fairly high incidence of mortality and disability. Most of these diseases are characterized by cardiac arrhythmias, conduction, and contractility disorders. Additionally, interruption of the electrical activity of the heart, the appearance of extensive ectopic foci, and heart failure are all symptoms of a number of severe hereditary diseases. The molecular mechanisms leading to the development of heart diseases are associated with impaired permeability and excitability of cell membranes and are mainly caused by the dysfunction of cardiac Ca2+ channels. Over the past 50 years, more than 100 varieties of ion channels have been found in the cardiovascular cells. The relationship between the activity of these channels and cardiac pathology, as well as the general cellular biological function, has been intensively studied on several cell types and experimental animal models in vivo and in situ. In this review, I discuss the origin of genetic Ca2+ channelopathies of L- and T-type voltage-gated calcium channels in humans and the role of the non-genetic dysfunctions of Ca2+ channels of various types: L-, R-, and T-type voltage-gated calcium channels, RyR2, including Ca2+ permeable nonselective cation hyperpolarization-activated cyclic nucleotide-gated (HCN), and transient receptor potential (TRP) channels, in the development of cardiac pathology in humans, as well as various aspects of promising experimental studies of the dysfunctions of these channels performed on animal models or in vitro.

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“…There is evidence of a wide involvement of TRP channels in the pathogenesis of CVD caused by hypoxia and oxidative stress, as well as ischemia-reperfusion (I/R) [90,104,[112][113][114].…”

Section: Ion Channels With Transient Receptor Potential (Trpc Trpm7 T...mentioning

confidence: 99%

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Shemarova

2023

IJMS

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show abstract

“…There is evidence of a wide involvement of TRP channels in the pathogenesis of CVD caused by hypoxia and oxidative stress, as well as ischemia-reperfusion (I/R) [90,104,[112][113][114].…”

Section: Ion Channels With Transient Receptor Potential (Trpc Trpm7 T...mentioning

confidence: 99%

Dysfunction of Ca2+ Channels in Hereditary and Chronic Cardiovascular Diseases

Шемарова¹

2023

Preprint

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Cardiovascular diseases (CVD) account for about 17.3 million annual deaths worldwide. 85% of these deaths occurred as a result of myocardial infarction (MI) and stroke. Chronic heart diseases, such as arterial hypertension (AH), coronary heart disease, various cerebrovascular diseases, dilated and hypertrophic cardiomyopathies are widespread, with a fairly high incidence of mortality and disability. Most of these diseases are characterized by cardiac arrhythmias, conduction and contractility disorders. Additionally, interruption of the electrical activity of the heart, the appearance of extensive ectopic foci and heart failure are all symptoms of a number of severe hereditary diseases. The molecular mechanisms leading to the development of CVD are associated with impaired permeability and excitability of cell membranes and mainly caused by dysfunction of cardiac Ca2+ channels. Acquired channelopathies are caused by metabolic disorders, increased tone of the sympathetic nervous system, age-related changes that lead to deterioration of coronary blood flow and hemodynamics. Currently known channelopathies, such as the long or short QT syndromes, Brugada and Lenegre syndromes, catecholaminergic polymorphic ventricular tachycardia, etc., are congenital and genetic disorders caused by mutations of genes "responsible" for the conductive properties of certain channel-forming proteins, including pore-forming subunits of Ca2+ channels. Over the past 50 years, more than 100 varieties of ion channels have been found in the cardiovascular system cells. The relationship between the activity of these channels and cardiac pathology, as well as the general cellular biological function, has been intensively studied on several cell types and experimental animal models in vivo и in situ. In this review, we discuss the origin of Ca2+ channelopathies and the role of Ca2+ channels of various types: L- R-, T-types voltage-gated calcium channels, RyR2, non-selective hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, transient receptor potential (TRPC, TRPM7, TRPA1) channels in the development of cardio-vascular pathology.

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Research Progress on TRPA1 in Diseases

Zhang

et al. 2023

J Membrane Biol

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For a long time, the physiological activity of TRP ion channels and the response to various stimuli have been the focus of attention, and the physiological functions mediated by ion channels have subtle links with the occurrence of various diseases. Our group has been engaged in the study of ion channels. In recent years, the report rate of TRPA1, the only member of the TRPA subfamily in the newly described TRP channel, has been very high. TRPA1 channels are not only abundantly expressed in peptidergic nociceptors but are also found in many nonneuronal cell types and tissues, and through the regulation of Ca2+ influx, various neuropeptides and signaling pathways are involved in the regulation of nerves, respiration, circulation, and various diseases and inflammation throughout the body. In this review, we mainly summarize the effects of TRPA1 on various systems in the body, which not only allows us to have a more systematic and comprehensive understanding of TRPA1 but also facilitates more in-depth research on it in the future. Graphical Abstract

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The effects of iloprost and beta3 receptor agonist on TRPA1 and TRPC1 immunreactivity in an experimental lower extremty ischemia-reperfusion injury model

Cited by 3 publications

References 27 publications

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models

Dysfunction of Ca2+ Channels in Hereditary and Chronic Cardiovascular Diseases

Research Progress on TRPA1 in Diseases

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