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Role of Transient Receptor Potential Vanilloid 4 in Vascular Function

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TLDR
Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed in systemic tissues and can be activated by many stimuli as mentioned in this paper, which can play an important role in the vasculature and is implicated in the regulation of cardiovascular homeostasis processes such as blood pressure, vascular remodeling, and pulmonary hypertension and edema.
Abstract
Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed in systemic tissues and can be activated by many stimuli. TRPV4, a Ca2+-permeable cation channel, plays an important role in the vasculature and is implicated in the regulation of cardiovascular homeostasis processes such as blood pressure, vascular remodeling, and pulmonary hypertension and edema. Within the vasculature, TRPV4 channels are expressed in smooth muscle cells, endothelial cells, and perivascular nerves. The activation of endothelial TRPV4 contributes to vasodilation involving nitric oxide, prostacyclin, and endothelial-derived hyperpolarizing factor pathways. TRPV4 activation also can directly cause vascular smooth muscle cell hyperpolarization and vasodilation. In addition, TRPV4 activation can evoke constriction in some specific vascular beds or under some pathological conditions. TRPV4 participates in the control of vascular permeability and vascular damage, particularly in the lung capillary endothelial barrier and lung injury. It also participates in vascular remodeling regulation mainly by controlling vasculogenesis and arteriogenesis. This review examines the role of TRPV4 in vascular function, particularly in vascular dilation and constriction, vascular permeability, vascular remodeling, and vascular damage, along with possible mechanisms, and discusses the possibility of targeting TRPV4 for therapy.

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Journal ArticleDOI

Reactive Oxygen Species and Endothelial Ca2+ Signaling: Brothers in Arms or Partners in Crime?

TL;DR: In this article, the authors survey how reactive oxygen species (ROS) induce endothelial Ca2+ signals to regulate vascular functions and, vice versa, how aberrant ROS generation may exploit the ca2+ handling machinery to promote endothelial dysfunction.
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Trpv protein family—from mechanosensing to cancer invasion

TL;DR: In this paper, the authors focus on the vanilloid family of TRP proteins and their connection to cancer progression through their mechanosensitive nature and show that they are critical components in the rapid transmission of physical signals into biologically compatible information to impact crucial processes during development and morphogenesis.
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Ca2+ Signalling and Hypoxia/Acidic Tumour Microenvironment Interplay in Tumour Progression

TL;DR: In this paper , the authors present an up-to-date and critical view on Ca2+ permeable ion channels, with a major focus on TRPs, SOCs and PIEZO channels, which are modulated by tumour hypoxia and acidosis.
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Transient receptor potential cation channel subfamily V (TRPV) and its importance in asthma.

TL;DR: In this article , the authors summarized the contribution of transient receptor potential (TRP) ion channels to the pathogenesis of asthma and proposed a novel biomarker for asthma in children, which may serve as novel therapeutic targets for this ailment.
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Calcium–Permeable Channels and Endothelial Dysfunction in Acute Lung Injury

TL;DR: This short review focuses on the up-to-date research and provides insight into the contribution of calcium influx via ion channels to the disruption of lung microvascular endothelial-barrier function during ALI.
References
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Journal ArticleDOI

Free Radicals in the Physiological Control of Cell Function

Wulf Dröge
TL;DR: There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
Journal ArticleDOI

The transient receptor potential family of ion channels

TL;DR: Mutations in several TRP genes have been implicated in diverse pathological states, including neurodegenerative disorders, skeletal dysplasia, kidney disorders and pain, and ongoing research may help find new therapies for treatments of related diseases.
Journal ArticleDOI

Cell swelling, heat, and chemical agonists use distinct pathways for the activation of the cation channel TRPV4.

TL;DR: It is demonstrated that blockers of phospholipase A2 (PLA2) and cytochrome P450 epoxygenase inhibit activation of TRPV4 by osmotic cell swelling but not by heat and 4α-phorbol 12,13-didecanoate, and it is concluded that TRpV4-activating stimuli promote channel opening by means of distinct pathways.
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Endothelium-Derived Hyperpolarizing Factor Where Are We Now?

TL;DR: The endothelium controls vascular tone not only by releasing nitric oxide and prostacyclin but also by other pathways causing hyperpolarization of the underlying smooth muscle cells, which can be evoked by direct electrical coupling through myo-endothelial junctions and/or the accumulation of potassium ions in the intercellular space.
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Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function

TL;DR: Results support the concept that Ca2+ influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca2- sensitivity of IK and SK channels to cause vasodilation.
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