Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy
Renal interstitial fibrosis (RIF) is a common pathological response in a broad range of prevalent chronic kidney diseases and ultimately leads to renal failure and death. Although RIF causes a high morbi-mortality worldwide, effective therapeutic drugs are urgently needed. Myofibroblasts are identif...
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doaj-34fb2263c2eb40f798c7e3677e93983d2021-06-03T04:54:47ZengElsevierBiomedicine & Pharmacotherapy0753-33222021-07-01139111386Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapyYa-long Feng0Wen-bo Wang1Yue Ning2Hua Chen3Pei Liu4School of Chemistry and Chemical Engineering, Xianyang Normal University, No.43 Wenlin Road, Xianyang 712000, Shaanxi, ChinaSchool of Chemistry and Chemical Engineering, Xianyang Normal University, No.43 Wenlin Road, Xianyang 712000, Shaanxi, China; Corresponding authors.School of Chemistry and Chemical Engineering, Xianyang Normal University, No.43 Wenlin Road, Xianyang 712000, Shaanxi, ChinaCollege of Pharmacy, Ningxia Medical University, No. 692 Shengli Road, Yinchuan, Ningxia 750003, China; Corresponding authors.Shaanxi Institute for Food and Drug Control, Xian, Shaanxi, 710065, ChinaRenal interstitial fibrosis (RIF) is a common pathological response in a broad range of prevalent chronic kidney diseases and ultimately leads to renal failure and death. Although RIF causes a high morbi-mortality worldwide, effective therapeutic drugs are urgently needed. Myofibroblasts are identified as the main effector during the process of RIF. Multiple types of cells, including fibroblasts, epithelial cells, endothelial cells, macrophages and pericytes, contribute to renal myofibroblasts origin, and lots of mediators, including signaling pathways (Transforming growth factor-β1, mammalian target of rapamycin and reactive oxygen species) and epigenetic modifications (Histone acetylation, microRNA and long non-coding RNA) are participated in renal myofibroblasts activation during renal fibrogenesis, suggesting that these mediators may be the promising targets for treating RIF. In addition, many small molecules show profound therapeutic effects on RIF by suppressing the origin and activation of renal myofibroblasts. Taken together, the review focuses on the mechanisms of the origin and activation of renal myofibroblasts in RIF and the small molecules against them improving RIF, which will provide a new insight for RIF therapy.http://www.sciencedirect.com/science/article/pii/S0753332221001712Renal interstitial fibrosisChronic kidney diseasesSmall moleculeNatural productMyofibroblast |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ya-long Feng Wen-bo Wang Yue Ning Hua Chen Pei Liu |
spellingShingle |
Ya-long Feng Wen-bo Wang Yue Ning Hua Chen Pei Liu Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy Biomedicine & Pharmacotherapy Renal interstitial fibrosis Chronic kidney diseases Small molecule Natural product Myofibroblast |
author_facet |
Ya-long Feng Wen-bo Wang Yue Ning Hua Chen Pei Liu |
author_sort |
Ya-long Feng |
title |
Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
title_short |
Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
title_full |
Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
title_fullStr |
Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
title_full_unstemmed |
Small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
title_sort |
small molecules against the origin and activation of myofibroblast for renal interstitial fibrosis therapy |
publisher |
Elsevier |
series |
Biomedicine & Pharmacotherapy |
issn |
0753-3322 |
publishDate |
2021-07-01 |
description |
Renal interstitial fibrosis (RIF) is a common pathological response in a broad range of prevalent chronic kidney diseases and ultimately leads to renal failure and death. Although RIF causes a high morbi-mortality worldwide, effective therapeutic drugs are urgently needed. Myofibroblasts are identified as the main effector during the process of RIF. Multiple types of cells, including fibroblasts, epithelial cells, endothelial cells, macrophages and pericytes, contribute to renal myofibroblasts origin, and lots of mediators, including signaling pathways (Transforming growth factor-β1, mammalian target of rapamycin and reactive oxygen species) and epigenetic modifications (Histone acetylation, microRNA and long non-coding RNA) are participated in renal myofibroblasts activation during renal fibrogenesis, suggesting that these mediators may be the promising targets for treating RIF. In addition, many small molecules show profound therapeutic effects on RIF by suppressing the origin and activation of renal myofibroblasts. Taken together, the review focuses on the mechanisms of the origin and activation of renal myofibroblasts in RIF and the small molecules against them improving RIF, which will provide a new insight for RIF therapy. |
topic |
Renal interstitial fibrosis Chronic kidney diseases Small molecule Natural product Myofibroblast |
url |
http://www.sciencedirect.com/science/article/pii/S0753332221001712 |
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