Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling

Singh, Rajvir; Kaundal, Ravinder K.; Zhao, Bei; Bouchareb, Rihab; Lebeche, Djamel

doi:10.1016/j.phrs.2020.105414

Cited by 37 publications

(21 citation statements)

References 54 publications

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“…Increased resistin expression can be detected in cardiac myocytes and CFs after myocardial infarction and in neurohumoral stimulation responses (145). Studies have shown that resistin gene knockout mice fed with high fat did not exhibit relevant changes in cardiac fibrosis (146). Cardiac tissue overexpressed with resistin presented all the major markers of fibroblasts as well as the phenotypic characteristic of fibrosis, and showed augmented expression of ECM proteins including a-SMA, COL1a1, CTGF/ CCN2, fibronectin, LOX, and SF2 (146).…”

Section: Abnormal Lipid Metabolism Affects Cardiac Fibroblastsmentioning

confidence: 99%

“…Studies have shown that resistin gene knockout mice fed with high fat did not exhibit relevant changes in cardiac fibrosis (146). Cardiac tissue overexpressed with resistin presented all the major markers of fibroblasts as well as the phenotypic characteristic of fibrosis, and showed augmented expression of ECM proteins including a-SMA, COL1a1, CTGF/ CCN2, fibronectin, LOX, and SF2 (146). Resistin stimulates the proliferation of adult mouse CFs, activates janus kinase 2 (JAK2) by binding to toll-like receptor 4 (TLR4), and then phosphorylates Stat3, which transfers to the nucleus and activates the expression of fibroblasts target genes (146).…”

Section: Abnormal Lipid Metabolism Affects Cardiac Fibroblastsmentioning

confidence: 99%

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Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

et al. 2023

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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.

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Section: Abnormal Lipid Metabolism Affects Cardiac Fibroblastsmentioning

confidence: 99%

Section: Abnormal Lipid Metabolism Affects Cardiac Fibroblastsmentioning

confidence: 99%

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

et al. 2023

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“…Indeed, Sun et al [90] found that hUC-MSCs overexpressing miR-455-5p augmented endometrial gland number and reduced fibrosis in a murine model with intrauterine adhesions. The authors argued that these regenerative processes were mediated by the activation of the JAK/STAT3 signaling pathway, which had previously been associated with cardiac subepithelial and hepatic fibrosis [222][223][224]. Alternatively, Zheng et al [93] transfected hUC-MSCs with miR-330-5p, combined the cells with a fibroin small-intestinal submucosa scaffold, and injected them into the damaged endometrial surface.…”

Section: Cellular Therapies Based On Huc-mscs: Current Applications A...mentioning

confidence: 99%

Human Umbilical Cord-Based Therapeutics: Stem Cells and Blood Derivatives for Female Reproductive Medicine

Rodríguez-Eguren

Gómez-Álvarez²,

Francés-Herrero

et al. 2022

IJMS

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There are several conditions that lead to female infertility, where traditional or conventional treatments have limited efficacy. In these challenging scenarios, stem cell (SC) therapies have been investigated as alternative treatment strategies. Human umbilical cord (hUC) mesenchymal stem cells (hUC-MSC), along with their secreted paracrine factors, extracts, and biomolecules, have emerged as promising therapeutic alternatives in regenerative medicine, due to their remarkable potential to promote anti-inflammatory and regenerative processes more efficiently than other autologous treatments. Similarly, hUC blood derivatives, such as platelet-rich plasma (PRP), or isolated plasma elements, such as growth factors, have also demonstrated potential. This literature review aims to summarize the recent therapeutic advances based on hUC-MSCs, hUC blood, and/or other plasma derivatives (e.g., extracellular vesicles, hUC-PRP, and growth factors) in the context of female reproductive medicine. We present an in-depth analysis of the principal molecules mediating tissue regeneration, compiling the application of these therapies in preclinical and clinical studies, within the context of the human reproductive tract. Despite the recent advances in bioengineering strategies that sustain delivery and amplify the scope of the therapeutic benefits, further clinical trials are required prior to the wide implementation of these alternative therapies in reproductive medicine.

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“…Matrix metalloproteinase 9 (MMP-9) could degrade the ECM and plays an important role in the compensation of myocardial fibrosis ( Medeiros et al, 2017 ). Signal transducer and activator of transcription 3 (STAT3), a member of STAT family, is a transcription factor, which can inhibit the degradation of ECM and regulate myocardial fibrosis ( Wang et al, 2019 ; Singh et al, 2021 ). Therefore, STAT3–MMP9 are promising antifibrosis targets for HF therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Calycosin as a Novel PI3K Activator Reduces Inflammation and Fibrosis in Heart Failure Through AKT–IKK/STAT3 Axis

Wang

Zhang

et al. 2022

Front. Pharmacol.

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Aim: Inflammation and fibrosis have been shown to be critical factors in heart failure (HF) progression. Calycosin (Cal) is the major active component of Astragalus mongholicus Bunge and has been reported to have therapeutic effects on the cardiac dysfunction after myocardial infarction. However, whether Cal could ameliorate myocardial infarction (MI)-induced inflammation and fibrosis and precise mechanisms remain uncertain. The aim of this study is to explore the role of Cal in HF and to clarify the underlying mechanisms.Methods: For in vivo experiments, rats underwent left anterior descending artery ligation for heart failure model, and the cardioprotective effects of Cal were measured by echocardiographic assessment and histological examination. RNA-seq approach was applied to explore potential differential genes and pathways. For further mechanistic study, proinflammatory-conditioned media (conditioned media)-induced H9C2 cell injury model and TGFβ-stimulated cardiac fibroblast model were applied to determine the regulatory mechanisms of Cal.Results: In the in vivo experiments, echocardiography results showed that Cal significantly improved heart function. GO and reactome enrichment revealed that inflammation and fibrosis pathways are involved in the Cal-treated group. KEGG enrichment indicated that the PI3K–AKT pathway is enriched in the Cal-treated group. Further experiments proved that Cal alleviated cardiomyocyte inflammatory responses evidenced by downregulating the expressions of phosphorylated IκB kinase α/β (p-IKKα/β), phosphorylated nuclear factor kapa B (p-NFκB), and tumor necrosis factor α (TNFα). Besides, Cal effectively attenuated cardiac fibrosis through the inhibitions of expressions and depositions of collagen I and collagen III. In the in vitro experiments, the phosphatidylinositol three kinase (PI3K) inhibitor LY294002 could abrogate the anti-inflammation and antifibrosis therapeutic effects of Cal, demonstrating that the cardioprotective effects of Cal were mediated through upregulations of PI3K and serine/threonine kinase (AKT).Conclusion: Cal inhibited inflammation and fibrosis via activation of the PI3K–AKT pathway in H9C2 cells, fibroblasts, and heart failure in postacute myocardial infarction rats.

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Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling

Cited by 37 publications

References 54 publications

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

Human Umbilical Cord-Based Therapeutics: Stem Cells and Blood Derivatives for Female Reproductive Medicine

Calycosin as a Novel PI3K Activator Reduces Inflammation and Fibrosis in Heart Failure Through AKT–IKK/STAT3 Axis

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