Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms

Fibrosis is a physiological response to organ injury and is characterized by the excessive deposition of connective tissue components in an organ, which results in the disruption of physiological architecture and organ remodeling, ultimately leading to organ failure and death. Fibrosis in the lung,...

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Main Authors: Maoyan Wu, Huiwen Xu, Jingyu Liu, Xiaozhen Tan, Shengrong Wan, Man Guo, Yang Long, Yong Xu
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2021/6673525
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author Maoyan Wu
Huiwen Xu
Jingyu Liu
Xiaozhen Tan
Shengrong Wan
Man Guo
Yang Long
Yong Xu
author_facet Maoyan Wu
Huiwen Xu
Jingyu Liu
Xiaozhen Tan
Shengrong Wan
Man Guo
Yang Long
Yong Xu
author_sort Maoyan Wu
collection DOAJ
description Fibrosis is a physiological response to organ injury and is characterized by the excessive deposition of connective tissue components in an organ, which results in the disruption of physiological architecture and organ remodeling, ultimately leading to organ failure and death. Fibrosis in the lung, kidney, and liver accounts for a substantial proportion of the global burden of disability and mortality. To date, there are no effective therapeutic strategies for controlling fibrosis. A class of metabolically targeted chemicals, such as adenosine monophosphate-activated protein kinase (AMPK) activators and peroxisome proliferator-activated receptor (PPAR) agonists, shows strong potential in fighting fibrosis. Metformin, which is a potent AMPK activator and is the only recommended first-line drug for the treatment of type 2 diabetes, has emerged as a promising method of fibrosis reduction or reversion. In this review, we first summarize the key experimental and clinical studies that have specifically investigated the effects of metformin on organ fibrosis. Then, we discuss the mechanisms involved in mediating the antifibrotic effects of metformin in depth.
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institution Kabale University
issn 2314-6745
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publishDate 2021-01-01
publisher Wiley
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series Journal of Diabetes Research
spelling doaj-art-f3422900bdbc417395441b3050b7d0702025-02-03T01:20:44ZengWileyJournal of Diabetes Research2314-67452314-67532021-01-01202110.1155/2021/66735256673525Metformin and Fibrosis: A Review of Existing Evidence and MechanismsMaoyan Wu0Huiwen Xu1Jingyu Liu2Xiaozhen Tan3Shengrong Wan4Man Guo5Yang Long6Yong Xu7Department of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, ChinaDepartment of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, ChinaSouthwest Medical University, Luzhou, Sichuan, 646000, ChinaCardiovascular and Metabolic Diseases Key Laboratory of Luzhou, Luzhou, Sichuan, 646000, ChinaDepartment of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, ChinaCardiovascular and Metabolic Diseases Key Laboratory of Luzhou, Luzhou, Sichuan, 646000, ChinaDepartment of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, ChinaDepartment of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, ChinaFibrosis is a physiological response to organ injury and is characterized by the excessive deposition of connective tissue components in an organ, which results in the disruption of physiological architecture and organ remodeling, ultimately leading to organ failure and death. Fibrosis in the lung, kidney, and liver accounts for a substantial proportion of the global burden of disability and mortality. To date, there are no effective therapeutic strategies for controlling fibrosis. A class of metabolically targeted chemicals, such as adenosine monophosphate-activated protein kinase (AMPK) activators and peroxisome proliferator-activated receptor (PPAR) agonists, shows strong potential in fighting fibrosis. Metformin, which is a potent AMPK activator and is the only recommended first-line drug for the treatment of type 2 diabetes, has emerged as a promising method of fibrosis reduction or reversion. In this review, we first summarize the key experimental and clinical studies that have specifically investigated the effects of metformin on organ fibrosis. Then, we discuss the mechanisms involved in mediating the antifibrotic effects of metformin in depth.http://dx.doi.org/10.1155/2021/6673525
spellingShingle Maoyan Wu
Huiwen Xu
Jingyu Liu
Xiaozhen Tan
Shengrong Wan
Man Guo
Yang Long
Yong Xu
Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
Journal of Diabetes Research
title Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
title_full Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
title_fullStr Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
title_full_unstemmed Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
title_short Metformin and Fibrosis: A Review of Existing Evidence and Mechanisms
title_sort metformin and fibrosis a review of existing evidence and mechanisms
url http://dx.doi.org/10.1155/2021/6673525
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AT xiaozhentan metforminandfibrosisareviewofexistingevidenceandmechanisms
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