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心脏成纤维细胞在糖尿病心肌病心肌纤维化中的核心作用。

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy.

机构信息

Beijing Key Laboratory of Diabetes Prevention and Research, Center for Endocrine Metabolic and Immune Diseases, Beijing Luhe Hospital, Capital Medical University, Beijing, China.

出版信息

Front Endocrinol (Lausanne). 2023 Mar 31;14:1162754. doi: 10.3389/fendo.2023.1162754. eCollection 2023.


DOI:10.3389/fendo.2023.1162754
PMID:37065745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10102655/
Abstract

Diabetic cardiomyopathy (DCM), a main cardiovascular complication of diabetes, can eventually develop into heart failure and affect the prognosis of patients. Myocardial fibrosis is the main factor causing ventricular wall stiffness and heart failure in DCM. Early control of myocardial fibrosis in DCM is of great significance to prevent or postpone the progression of DCM to heart failure. A growing body of evidence suggests that cardiomyocytes, immunocytes, and endothelial cells involve fibrogenic actions, however, cardiac fibroblasts, the main participants in collagen production, are situated in the most central position in cardiac fibrosis. In this review, we systematically elaborate the source and physiological role of myocardial fibroblasts in the context of DCM, and we also discuss the potential action and mechanism of cardiac fibroblasts in promoting fibrosis, so as to provide guidance for formulating strategies for prevention and treatment of cardiac fibrosis in DCM.

摘要

糖尿病心肌病(DCM)是糖尿病的主要心血管并发症,最终可发展为心力衰竭并影响患者的预后。心肌纤维化是 DCM 导致心室壁僵硬和心力衰竭的主要因素。早期控制 DCM 中的心肌纤维化对于预防或延缓 DCM 向心力衰竭的进展具有重要意义。越来越多的证据表明,心肌细胞、免疫细胞和内皮细胞参与成纤维作用,然而,心肌成纤维细胞是胶原产生的主要参与者,位于心肌纤维化的最中心位置。在这篇综述中,我们系统地阐述了 DCM 背景下心肌成纤维细胞的来源和生理作用,还讨论了心肌成纤维细胞在促进纤维化中的潜在作用和机制,以期为制定 DCM 中心肌纤维化的防治策略提供指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/512757df1e2a/fendo-14-1162754-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/b2629d437158/fendo-14-1162754-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/4bd3687c0741/fendo-14-1162754-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/4ad0402992f9/fendo-14-1162754-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/512757df1e2a/fendo-14-1162754-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/b2629d437158/fendo-14-1162754-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/4bd3687c0741/fendo-14-1162754-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/4ad0402992f9/fendo-14-1162754-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23bc/10102655/512757df1e2a/fendo-14-1162754-g004.jpg

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Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy.

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[2]
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[3]
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[5]
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[6]
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[7]
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[8]
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J Cardiothorac Surg. 2025-3-29

[9]
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[10]
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本文引用的文献

[1]
The interplay of inflammation, exosomes and Ca dynamics in diabetic cardiomyopathy.

Cardiovasc Diabetol. 2023-2-20

[2]
Single-cell analysis reveals lysyl oxidase (Lox) fibroblast subset involved in cardiac fibrosis of diabetic mice.

J Adv Res. 2023-12

[3]
Metformin Attenuates Hyperglycaemia-Stimulated Pro-Fibrotic Gene Expression in Adventitial Fibroblasts via Inhibition of Discoidin Domain Receptor 2.

Int J Mol Sci. 2022-12-29

[4]
Unveiling the Vital Role of Long Non-Coding RNAs in Cardiac Oxidative Stress, Cell Death, and Fibrosis in Diabetic Cardiomyopathy.

Antioxidants (Basel). 2022-12-1

[5]
Docosahexaenoic acid administration improves diabetes-induced cardiac fibrosis through enhancing fatty acid oxidation in cardiac fibroblast.

J Nutr Biochem. 2023-3

[6]
Fibroblast-specific activation of Rnd3 protects against cardiac remodeling in diabetic cardiomyopathy via suppression of Notch and TGF-β signaling.

Theranostics. 2022

[7]
Silencing RIPK1/mTORC1 signalling attenuated the inflammation and oxidative stress in diabetic cardiomyopathy.

Exp Cell Res. 2023-1-15

[8]
Research status and trends of the diabetic cardiomyopathy in the past 10 years (2012-2021): A bibliometric analysis.

Front Cardiovasc Med. 2022-10-20

[9]
ADAM17 knockdown mitigates while ADAM17 overexpression aggravates cardiac fibrosis and dysfunction regulating ACE2 shedding and myofibroblast transformation.

Front Pharmacol. 2022-10-14

[10]
NOX1 promotes myocardial fibrosis and cardiac dysfunction activating the TLR2/NF-κB pathway in diabetic cardiomyopathy.

Front Pharmacol. 2022-9-26

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