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TRPV4 Mechanotransduction in Fibrosis
Fibrosis is an irreversible, debilitating condition marked by the excessive production of extracellular matrix and tissue scarring that eventually results in organ failure and disease. Differentiation of fibroblasts to hypersecretory myofibroblasts is the key event in fibrosis. Although both soluble...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8619244/ https://www.ncbi.nlm.nih.gov/pubmed/34831281 http://dx.doi.org/10.3390/cells10113053 |
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author | Adapala, Ravi K. Katari, Venkatesh Teegala, Lakshminarayan Reddy Thodeti, Sathwika Paruchuri, Sailaja Thodeti, Charles K. |
author_facet | Adapala, Ravi K. Katari, Venkatesh Teegala, Lakshminarayan Reddy Thodeti, Sathwika Paruchuri, Sailaja Thodeti, Charles K. |
author_sort | Adapala, Ravi K. |
collection | PubMed |
description | Fibrosis is an irreversible, debilitating condition marked by the excessive production of extracellular matrix and tissue scarring that eventually results in organ failure and disease. Differentiation of fibroblasts to hypersecretory myofibroblasts is the key event in fibrosis. Although both soluble and mechanical factors are implicated in fibroblast differentiation, much of the focus is on TGF-β signaling, but to date, there are no specific drugs available for the treatment of fibrosis. In this review, we describe the role for TRPV4 mechanotransduction in cardiac and lung fibrosis, and we propose TRPV4 as an alternative therapeutic target for fibrosis. |
format | Online Article Text |
id | pubmed-8619244 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-86192442021-11-27 TRPV4 Mechanotransduction in Fibrosis Adapala, Ravi K. Katari, Venkatesh Teegala, Lakshminarayan Reddy Thodeti, Sathwika Paruchuri, Sailaja Thodeti, Charles K. Cells Review Fibrosis is an irreversible, debilitating condition marked by the excessive production of extracellular matrix and tissue scarring that eventually results in organ failure and disease. Differentiation of fibroblasts to hypersecretory myofibroblasts is the key event in fibrosis. Although both soluble and mechanical factors are implicated in fibroblast differentiation, much of the focus is on TGF-β signaling, but to date, there are no specific drugs available for the treatment of fibrosis. In this review, we describe the role for TRPV4 mechanotransduction in cardiac and lung fibrosis, and we propose TRPV4 as an alternative therapeutic target for fibrosis. MDPI 2021-11-06 /pmc/articles/PMC8619244/ /pubmed/34831281 http://dx.doi.org/10.3390/cells10113053 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Adapala, Ravi K. Katari, Venkatesh Teegala, Lakshminarayan Reddy Thodeti, Sathwika Paruchuri, Sailaja Thodeti, Charles K. TRPV4 Mechanotransduction in Fibrosis |
title | TRPV4 Mechanotransduction in Fibrosis |
title_full | TRPV4 Mechanotransduction in Fibrosis |
title_fullStr | TRPV4 Mechanotransduction in Fibrosis |
title_full_unstemmed | TRPV4 Mechanotransduction in Fibrosis |
title_short | TRPV4 Mechanotransduction in Fibrosis |
title_sort | trpv4 mechanotransduction in fibrosis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8619244/ https://www.ncbi.nlm.nih.gov/pubmed/34831281 http://dx.doi.org/10.3390/cells10113053 |
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