Jatrorrhizine reduces myocardial infarction-induced apoptosis and fibrosis through inhibiting p53 and TGF-β1/Smad2/3 pathways in mice

Hao, Mingxiu; Jiao, Kunli

doi:10.1590/acb370705

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…TGF-β/Smad2/3 is one of the important mechanisms that cause cardiac brosis [31][32][33]. TGF-β, as a cytokine, promotes MCF activation and extracellular matrix production and plays a key role in cardiac brosis [34].…”

Section: Discussionmentioning

confidence: 99%

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

Tan

Wei²,

2022

Preprint

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Soluble interleukin 1 receptor-like 1 (sST2) is a novel predictor of poor outcomes, which is involved in inflammatory response and fibrosis of myocarditis. Cardiac fibrosis is a major cause of cardiovascular disease. Cellular senescence is a state of irreversible cell cycle arrest and studies have shown that senescence of myofibroblasts can limit or reduce myocardial fibrosis. Previous studies show that cellular senescence is associated with the progress of myocarditis, and cardiac fibroblasts is closely related to cardiac fibrosis. Therefore, we investigated the role of sST2 on senescence and fibrosis in mice cardiac fibroblasts (MCF). Meanwhile, its pathological role in mice viral myocarditis (VMC) was also investigated. In vitro experiments revealed that sST2 is beneficial to activate MCF by TGF-β1/Smad2/3 signaling and inhibit cell senescence by Sirt1/P53/P21 signaling pathway. CVB3-infected mice exhibited an increased deposition of collagen in the heart and decreased MCF senescence compared to WT mice while these pathological effects are reversed by anti-ST2 mAb. In addition, we found that inhibiting the senescence of MCF is beneficial to cardiac fibrosis and this effect is achieved by paracrine action. The present study reveals a new pathogenic pathway, sST2, which leads to cardiac fibrosis of VMC by inhibiting MCF senescence.

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Section: Discussionmentioning

confidence: 99%

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

Tan

Wei²,

2022

Preprint

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“…Calycosin and taohong siwu decoction suppress TGF-β1-induced CFs proliferation and collagen deposition ( Tan et al, 2021 ; Chen et al, 2022a ). Moreover, zerumbone, ganxin V, nutmeg-5, ginsenoside Rg2, jatrorrhizine, cardiotonic pill, and huoxin pill all regulate the TGF-β1/smad pathway to attenuate fibrosis ( Li et al, 2020d ; Wang et al, 2021b ; Yan et al, 2022a ; Yan et al, 2022b ; Li et al, 2022c ; Hao and Jiao, 2022 ; Liang et al, 2022 ). Moreover, citri reticulatae pericarpium also reduces CMs apoptosis, CFs proliferation, and CF-to-MF transformation by upregulating PPAR-γ expression ( Chen et al, 2022c ), while auraptene improves cardiac hypertrophy and dysfunction via activating PPARα ( Sunagawa et al, 2022b ).…”

Section: Interventions For Cardiac Fibrosismentioning

confidence: 99%

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Yin

Pan

et al. 2023

Front. Pharmacol.

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Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI). The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways and various types of cells in time-dependent manners. Our understanding of the development of cardiac fibrosis after MI has evolved in basic and clinical researches, and the regulation of fibrotic remodeling may facilitate novel diagnostic and therapeutic strategies, and finally improve outcomes. Here, we aim to elaborate pathophysiology, examination and intervention of cardiac fibrosis after MI.

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“…Inhibition of the TGF-β1 signaling pathway can significantly ameliorate myocardial fibrosis in DCM [ 16 ]. Mothers Against decapentaplegic homolog 7 (Smad7) is a crucial negative feedback factor in the TGF-β1 signaling pathway [ 17 , 18 ]. Smad7 can block the TGF-β1 signaling pathway by inhibiting the phosphorylation of receptor-regulated Smads, such as Smad3 [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7

Luo,

Fu,

Wang

et al. 2023

Chin Med

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Background Salvianolic acid B (Sal B), a water-soluble phenolic compound derived from Salvia miltiorrhiza Bunge, is commonly used in Traditional Chinese Medicine to treat cardiovascular disease. In our previous study, Sal B protected against myocardial fibrosis induced by diabetic cardiomyopathy (DCM). This study aimed to investigate the ameliorative effects and potential mechanisms of Sal B in mitigating myocardial fibrosis induced by DCM. Methods Various methods were used to investigate the effects of Sal B on myocardial fibrosis induced by DCM in vivo and in vitro. These methods included blood glucose measurement, echocardiography, HE staining, Masson’s trichrome staining, Sirius red staining, cell proliferation assessment, determination of hydroxyproline levels, immunohistochemical staining, evaluation of fibrosis-related protein expression (Collagen-I, Collagen-III, TGF-β1, p-Smad3, Smad3, Smad7, and α-smooth muscle actin), analysis of Smad7 gene expression, and analysis of Smad7 ubiquitin modification. Results The animal test results indicated that Sal B significantly improved cardiac function, inhibited collagen deposition and phenotypic transformation, and ameliorated myocardial fibrosis in DCM by upregulating Smad7, thereby inhibiting the TGF-β1 signaling pathway. In addition, cell experiments demonstrated that Sal B significantly inhibited the proliferation, migration, phenotypic transformation, and collagen secretion of cardiac fibroblasts (CFs) induced by high glucose (HG). Sal B significantly decreased the ubiquitination of Smad7 and stabilized the protein expression of Smad7, thereby increasing the protein expression of Smad7 in CFs and inhibiting the TGF-β1 signaling pathway, which may be the potential mechanism by which Sal B mitigates myocardial fibrosis induced by DCM. Conclusion This study revealed that Sal B can improve myocardial fibrosis in DCM by deubiquitinating Smad7, stabilizing the protein expression of Smad7, and blocking the TGF-β1 signaling pathway.

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Jatrorrhizine reduces myocardial infarction-induced apoptosis and fibrosis through inhibiting p53 and TGF-β1/Smad2/3 pathways in mice

Cited by 7 publications

References 23 publications

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7

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