Transient receptor potential channels in cardiac health and disease

Hof, Thomas; Chaigne, Sébastien; Récalde, Alice; Sallé, Laurent; Brette, Fabien; Guinamard, Romain

doi:10.1038/s41569-018-0145-2

Cited by 102 publications

(87 citation statements)

References 164 publications

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“…The expression of TRPC isoforms in the heart was examined in different stages of animal development, animal models, and areas of the heart. They are expressed at very low levels in normal adult cardiac myocytes but their expression and activity might increase in pathological processes [12,13,27]. However, they likely display different patterns of expression in cardiac cells isolated from the sinoatrial node and in myocytes isolated from atrial or ventricular heart [22,28].…”

Section: Trpc Channels In the Cardiovascular Systemmentioning

confidence: 99%

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

Falcón

Galeano-Otero

Martín-Bórnez

et al. 2020

Cells

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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca2+ concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.

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Section: Trpc Channels In the Cardiovascular Systemmentioning

confidence: 99%

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

Falcón

Galeano-Otero

Martín-Bórnez

et al. 2020

Cells

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“…The calcium-permeable ion channel transient receptor potential vanilloid subfamily 4 (TRPV4) is expressed in various tissues and cells (e.g., smooth muscle of the urinary bladder, epithelial cells of kidney, airways, sensory neurons, and vascular endothelium) and is involved in several physiological processes and diseases, including regulation of blood flow, shear-induced vasodilation, and epithelial ciliary activity (30)(31)(32)(33)(34)(35)(36)(37). TRPV4-mediated pathological events include neurogenic inflammation, hyperalgesia, endothelial dysfunction, and pulmonary and cardiac tissue fibrosis (33,36,(38)(39)(40).…”

Section: Introductionmentioning

confidence: 99%

TRPV4 channel opening mediates pressure-induced pancreatitis initiated by Piezo1 activation

Swain

Romac

Shahid

et al. 2020

Journal of Clinical Investigation

136

127

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“…Recently, it was demonstrated via quantitative high-resolution mass spectrometry analysis using subtype specific antibodies that TRPC1, TRPC4, and TRPC5 form heteromultimers with each other but not with other TRP family members in the mouse brain and hippocampus [45]. Corresponding analyses in other tissues including the heart were not reported yet, although numerous studies reported their expression and function in cardiomyocytes but also in non-myocytes including cultured fibroblasts [46][47][48][49][50][51][52].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

Londoño

Marx

Kraft

et al. 2020

Cells

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TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.

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Transient receptor potential channels in cardiac health and disease

Cited by 102 publications

References 164 publications

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

TRPV4 channel opening mediates pressure-induced pancreatitis initiated by Piezo1 activation

Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

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