Diabetic fibrosis.
Diabetes
Extracellular matrix
Fibroblast
Fibrosis
Growth factors
Matricellular proteins
Journal
Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730
Informations de publication
Date de publication:
01 04 2021
01 04 2021
Historique:
received:
13
08
2020
revised:
25
11
2020
accepted:
07
12
2020
pubmed:
31
12
2020
medline:
3
7
2021
entrez:
30
12
2020
Statut:
ppublish
Résumé
Diabetes-associated morbidity and mortality is predominantly due to complications of the disease that may cause debilitating conditions, such as heart and renal failure, hepatic insufficiency, retinopathy or peripheral neuropathy. Fibrosis, the excessive and inappropriate deposition of extracellular matrix in various tissues, is commonly found in patients with advanced type 1 or type 2 diabetes, and may contribute to organ dysfunction. Hyperglycemia, lipotoxic injury and insulin resistance activate a fibrotic response, not only through direct stimulation of matrix synthesis by fibroblasts, but also by promoting a fibrogenic phenotype in immune and vascular cells, and possibly also by triggering epithelial and endothelial cell conversion to a fibroblast-like phenotype. High glucose stimulates several fibrogenic pathways, triggering reactive oxygen species generation, stimulating neurohumoral responses, activating growth factor cascades (such as TGF-β/Smad3 and PDGFs), inducing pro-inflammatory cytokines and chemokines, generating advanced glycation end-products (AGEs) and stimulating the AGE-RAGE axis, and upregulating fibrogenic matricellular proteins. Although diabetes-activated fibrogenic signaling has common characteristics in various tissues, some organs, such as the heart, kidney and liver develop more pronounced and clinically significant fibrosis. This review manuscript summarizes current knowledge on the cellular and molecular pathways involved in diabetic fibrosis, discussing the fundamental links between metabolic perturbations and fibrogenic activation, the basis for organ-specific differences, and the promises and challenges of anti-fibrotic therapies for diabetic patients.
Identifiants
pubmed: 33378699
pii: S0925-4439(20)30392-6
doi: 10.1016/j.bbadis.2020.166044
pmc: PMC7867637
mid: NIHMS1658074
pii:
doi:
Substances chimiques
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
166044Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL085440
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL149407
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL076246
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020541
Pays : United States
Organisme : NIDDK NIH HHS
ID : P60 DK020541
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.
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