4.5 Article

Physiological levels of fluid shear stress modulate vascular function through TRPV4 sparklets

相关参考文献

注意:仅列出部分参考文献,下载原文获取全部文献信息。
Article Pharmacology & Pharmacy

Endothelial TRPV4-eNOS coupling as a vital therapy target for treatment of hypertension

Aiqin Mao et al.

Summary: This study used single-cell RNA-sequencing, single-cell functional study, and drug screening to identify a subpopulation of CD106(+) TRPV4(high)NOS3(high) endothelial cells (ECs) in the aorta. The impaired TRPV4-eNOS interaction was found to be important in the progression of hypertension, and a small molecule drug, JNc-463, was designed to improve this interaction. This research provides valuable insights into endothelial dysfunction and offers potential therapeutic targets for treating hypertension.

BRITISH JOURNAL OF PHARMACOLOGY (2022)

Article Cardiac & Cardiovascular Systems

Omega-3 fatty acids improve flow-induced vasodilation by enhancing TRPV4 in arteries from diet-induced obese mice

Yifei Zhu et al.

Summary: Omega-3 can improve vascular function in obese mice induced by a high-fat diet by enhancing TRPV4 activity, which leads to improved flow-induced vasodilation.

CARDIOVASCULAR RESEARCH (2021)

Article Biochemistry & Molecular Biology

Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

Sandip M. Swain et al.

Summary: Both Piezo1 and TRPV4 ion channels are independently implicated in high venous pressure- and fluid shear stress-induced vascular hyperpermeability in endothelial cells. Piezo1 regulates TRPV4 channel activation in endothelial cells, with TRPV4 opening being dependent on the strength and duration of fluid shear stress. The deleterious effects initiated by Piezo1 in response to shear stress require the involvement of TRPV4 channels, as demonstrated by the calcium signaling and disruption of cellular integrity observed in endothelial cells.

JOURNAL OF BIOLOGICAL CHEMISTRY (2021)

Article Multidisciplinary Sciences

Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension

Zdravka Daneva et al.

Summary: Recent studies have found that the activity of TRPV4 channels in endothelial cell caveolae is impaired in patients with pulmonary hypertension and mouse models. Up-regulation of iNOS and NOX1 enzymes leads to the formation of the oxidant molecule peroxynitrite, which targets the structural protein caveolin-1 and reduces the activity of TRPV4 channels.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2021)

Article Biology

Endothelial pannexin 1-TRPV4 channel signaling lowers pulmonary arterial pressure in mice

Zdravka Daneva et al.

Summary: The study showed that endothelial Panx1 signaling pathway contributes to vasodilation and reduces pulmonary arterial pressure through ATP-TRPV4 channel signaling. By regulating ATP efflux and TRPV4 channel activity, Panx1 could potentially be targeted for the treatment of pulmonary arterial hypertension and related diseases.
Article Multidisciplinary Sciences

TRPC1 participates in the HSV-1 infection process by facilitating viral entry

DongXu He et al.

SCIENCE ADVANCES (2020)

Article Pharmacology & Pharmacy

Shear stress sensitizes TRPV4 in endothelium-dependent vasodilatation

William G. Darby et al.

PHARMACOLOGICAL RESEARCH (2018)

Article Medicine, Research & Experimental

Treatment of hypertension by increasing impaired endothelial TRPV4-KCa2.3 interaction

Dongxu He et al.

EMBO MOLECULAR MEDICINE (2017)

Article Hematology

Shear Stress-Initiated Signaling and Its Regulation of Endothelial Function

Jing Zhou et al.

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY (2014)

Article Biochemistry & Molecular Biology

TRPV4, TRPC1, and TRPP2 assemble to form a flow-sensitive heteromeric channel

Juan Du et al.

FASEB JOURNAL (2014)

Article Multidisciplinary Sciences

Elementary Ca2+ Signals Through Endothelial TRPV4 Channels Regulate Vascular Function

Swapnil K. Sonkusare et al.

SCIENCE (2012)

Article Cardiac & Cardiovascular Systems

TRPV4-mediated endothelial Ca2+ influx and vasodilation in response to shear stress

Suelhem A. Mendoza et al.

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY (2010)

Review Biochemistry & Molecular Biology

The vanilloid transient receptor potential channel TRPV4: From structure to disease

Wouter Everaerts et al.

PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY (2010)

Article Cardiac & Cardiovascular Systems

TRPC1 Associates With BKCa Channel to Form a Signal Complex in Vascular Smooth Muscle Cells

Hiu-Yee Kwan et al.

CIRCULATION RESEARCH (2009)

Article Cardiac & Cardiovascular Systems

Role of cytochrome P450-dependent transient receptor potential V4 activation in flow-induced vasodilatation

Annemarieke E. Loot et al.

CARDIOVASCULAR RESEARCH (2008)

Article Multidisciplinary Sciences

Functional architecture of inositol 1,4,5-trisphosphate signaling in restricted spaces of myoendothelial projections

Jonathan Ledoux et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2008)

Article Multidisciplinary Sciences

Arterial Response to Shear Stress Critically Depends on Endothelial TRPV4 Expression

Veronika Hartmannsgruber et al.

PLOS ONE (2007)

Article Multidisciplinary Sciences

G protein-coupled receptors sense fluid shear stress in endothelial cells

Mirianas Chachisvilis et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2006)

Article Hematology

Evidence for a functional role of endothelial transient receptor potential V4 in shear stress-induced vasodilatation

Ralf Koehler et al.

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY (2006)

Review Medicine, Research & Experimental

The role of shear stress in the pathogenesis of atherosclerosis

KS Cunningham et al.

LABORATORY INVESTIGATION (2005)

Article Cardiac & Cardiovascular Systems

Shear stress-induced up-regulation of the intermediate-conductance Ca2+-activated K+ channel in human endothelium

S Brakemeier et al.

CARDIOVASCULAR RESEARCH (2003)