Journal ArticleDOI
Irisin attenuates angiotensin II-induced cardiac fibrosis via Nrf2 mediated inhibition of ROS/ TGFβ1/Smad2/3 signaling axis
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TLDR
It is found that angiotensin II-induced cardiac dysfunction and fibrotic responses were dampened by irisin treatment in mice, and irisin is identified as a promising anti-fibrotic therapeutic for angioten II-related cardiac fibrosis.About:
This article is published in Chemico-Biological Interactions.The article was published on 2019-04-01. It has received 55 citations till now. The article focuses on the topics: Angiotensin II & Cardiac fibrosis.read more
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Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D.
Natalia de las Heras,Virna Margarita Martín Giménez,León Ferder,Walter Manucha,Vicente Lahera +4 more
TL;DR: The purpose of this review is to deepen the knowledge about the role of mitochondria and vitamin D directly involved in the regulation of oxidative stress and the inflammatory state in SARS-CoV-2 infection.
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Bergenin impedes the generation of extracellular matrix in glomerular mesangial cells and ameliorates diabetic nephropathy in mice by inhibiting oxidative stress via the mTOR/β-TrcP/Nrf2 pathway
Simiao Qiao,Rui Liu,Changjun Lv,Yumeng Miao,Mengfan Yue,Yu Tao,Zhifeng Wei,Yufeng Xia,Yue Dai +8 more
TL;DR: Bergenin can inhibit glucose-induced ECM production in glomerular mesangial cells through the down-regulation of oxidative stress via the mTOR/β-TrcP/Nrf2 pathway, and it might be a candidate drug for the prevention and treatment of DN.
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Induction of LOX by TGF-β1/Smad/AP-1 signaling aggravates rat myocardial fibrosis and heart failure.
TL;DR: LOX can be induced by TGF‐β1/Smad/AP‐1 signaling and LOX inhibition attenuates rat myocardial fibrosis and CHF, and inhibition of LOX by β‐aminopropionitrile (BAPN) mitigated the RAAS activation and attenuated cardiac dysfunction, ventricular remodeling, myocardian fibrosis, and collagen deposition in CHF rats.
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Recombinant Irisin Prevents the Reduction of Osteoblast Differentiation Induced by Stimulated Microgravity through Increasing β-Catenin Expression.
Zhihao Chen,Yan Zhang,Fan Zhao,Chong Yin,Chaofei Yang,Xue Wang,Zixiang Wu,Shujing Liang,Dijie Li,Xiao Lin,Ye Tian,Lifang Hu,Yu Li,Airong Qian +13 more
TL;DR: This study is the first to show that r-irisin positively regulates osteoblast differentiation under simulated microgravity through increasing β-catenin expression, which may reveal a novel mechanism, and it provides a prevention strategy for bone loss and muscle atrophy induced by microgravity.
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Icariin Prevents Extracellular Matrix Accumulation and Ameliorates Experimental Diabetic Kidney Disease by Inhibiting Oxidative Stress via GPER Mediated p62-Dependent Keap1 Degradation and Nrf2 Activation.
TL;DR: It is demonstrated that the therapeutic effects of icariin on type 1 diabetic nephropathy in rats via GPER mediated p62-dependent Keap1 degradation and Nrf2 activation and the GPER antagonist G15 and siGPER obviously abolished the above effects by icARIin.
References
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Journal ArticleDOI
Cardiac Fibrosis: The Fibroblast Awakens.
TL;DR: Current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury are summarized, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis are summarized.
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Pivotal role of a gp91(phox)-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice.
TL;DR: A gp91phox-containing NADPH oxidase plays an important role in the development of angiotensin II-induced cardiac hypertrophy, independent of changes in blood pressure.
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Angiotensin II Blockade Reverses Myocardial Fibrosis in a Transgenic Mouse Model of Human Hypertrophic Cardiomyopathy
Do Sun Lim,Silvia Lutucuta,Pavan Bachireddy,Keith A. Youker,Alida J. Evans,Mark L. Entman,Robert Roberts,Ali J. Marian +7 more
TL;DR: It is suggested that losartan has the potential to reverse or attenuate interstitial fibrosis, a major predictor of sudden cardiac death, in human patients with HCM.
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Getting to the Heart of the Matter: New Insights Into Cardiac Fibrosis
TL;DR: This review addresses the contribution of a complex signaling network involving transforming growth factor-β, endothelin-1, angiotensin II, CCN2 (connective tissue growth factor), and platelet-derived growth factor to cardiac fibrosis.
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Aldosterone mediates angiotensin II-induced interstitial cardiac fibrosis via a Nox2-containing NADPH oxidase
TL;DR: In this article, the potential role of a Nox2-containing NADPH oxidase in aldosterone-induced fibrosis and the involvement of this mechanism in AngII-induced effects was investigated.