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Your search keyword '"cardiac fibrosis"' showing total 2 results
2 results on '"cardiac fibrosis"'

1. Targeting Interactions between Fibroblasts and Macrophages to Treat Cardiac Fibrosis.

Author

Yang, Bo, Qiao, Yan, Yan, Dong, and Meng, Qinghang

Subjects
*HEART fibrosis, *FIBROBLASTS, *MACROPHAGES, *EXTRACELLULAR matrix, *HYPERTROPHIC scars, *PHYSIOLOGY
Abstract

Excessive extracellular matrix (ECM) deposition is a defining feature of cardiac fibrosis. Most notably, it is characterized by a significant change in the concentration and volume fraction of collagen I, a disproportionate deposition of collagen subtypes, and a disturbed ECM network arrangement, which directly affect the systolic and diastolic functions of the heart. Immune cells that reside within or infiltrate the myocardium, including macrophages, play important roles in fibroblast activation and consequent ECM remodeling. Through both direct and indirect connections to fibroblasts, monocyte-derived macrophages and resident cardiac macrophages play complex, bidirectional, regulatory roles in cardiac fibrosis. In this review, we discuss emerging interactions between fibroblasts and macrophages in physiology and pathologic conditions, providing insights for future research aimed at targeting macrophages to combat cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction

Author

Qiaoqin Liang, Yixin Kuang, Wenfei Zhu, Yixuan Ma, Mengxin Cai, Wenyan Bo, and Zhenjun Tian

Subjects
Male, FGF21, Cardiac fibrosis, cardiac fibrosis, Myocardial Infarction, Apoptosis, Smad2 Protein, medicine.disease_cause, Mice, Fibrosis, Myocardial infarction, Biology (General), Spectroscopy, Cells, Cultured, Mice, Knockout, General Medicine, Recombinant Proteins, Computer Science Applications, Exercise Therapy, Chemistry, Matrix Metalloproteinase 9, Matrix Metalloproteinase 2, Signal Transduction, Cardiac function curve, medicine.medical_specialty, QH301-705.5, fibroblast growth factor 21, Catalysis, Article, Inorganic Chemistry, Transforming Growth Factor beta1, Internal medicine, medicine, Aerobic exercise, Animals, Smad3 Protein, Physical and Theoretical Chemistry, QD1-999, Molecular Biology, business.industry, Myocardium, Organic Chemistry, Fibroblasts, medicine.disease, Fibroblast Growth Factors, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, business, exercise training, Oxidative stress, Transforming growth factor
Abstract

Exercise training has been reported to alleviate cardiac fibrosis and ameliorate heart dysfunction after myocardial infarction (MI), but the molecular mechanism is still not fully clarified. Fibroblast growth factor 21 (FGF21) exerts a protective effect on the infarcted heart. This study investigates whether exercise training could increase FGF21 protein expression and regulate the transforming growth factor-β1 (TGF-β1)-Smad2/3-MMP2/9 signaling pathway to alleviate cardiac fibrosis following MI. Male wild type (WT) C57BL/6J mice and Fgf21 knockout (Fgf21 KO) mice were used to establish the MI model and subjected to five weeks of different types of exercise training. Both aerobic exercise training (AET) and resistance exercise training (RET) significantly alleviated cardiac dysfunction and fibrosis, up-regulated FGF21 protein expression, inhibited the activation of TGF-β1-Smad2/3-MMP2/9 signaling pathway and collagen production, and meanwhile, enhanced antioxidant capacity and reduced cell apoptosis in the infarcted heart. In contrast, knockout of Fgf21 weakened the cardioprotective effects of AET after MI. In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H2O2 (100 μM, 6 h). Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H2O2-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production. In conclusion, exercise training increases FGF21 protein expression, inactivates the TGF-β1-Smad2/3-MMP2/9 signaling pathway, alleviates cardiac fibrosis, oxidative stress, and cell apoptosis, and finally improves cardiac function in mice with MI. FGF21 plays an important role in the anti-fibrosis effect of exercise training.

Published
2021

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