CTRP3 attenuates post-infarct cardiac fibrosis by targeting Smad3 activation and inhibiting myofibroblast differentiation

Wu, Dan; Lei, Hong; Wang, Jinyu; Zhang, Chenglin; Feng, Han‐Zhong; Fu, Feng-Ying; Li, Li; Wu, Li‐Ling

doi:10.1007/s00109-015-1309-8

Cited by 82 publications

(84 citation statements)

References 49 publications

(60 reference statements)

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“…CTRP3 has a 28% amino acid identity with adiponectin 320 , and supplementation of this adipokine has been reported to improve cardiac function and reduce fibrosis in mice after myocardial infarction, which is accompanied by increased capillary density and decreased apoptosis in ischemic areas of the heart 324, 325 . In vitro , CTRP3 inhibits TGF-β-induced profibrotic gene expression in cardiac fibroblasts 325 and promotes cardiac myocyte survival and VEGF-A expression through its ability to activate an Akt/HIF-1α-dependent pathway.…”

Section: Cardiovascular Actions Of Select Adipokinesmentioning

confidence: 99%

“…In vitro , CTRP3 inhibits TGF-β-induced profibrotic gene expression in cardiac fibroblasts 325 and promotes cardiac myocyte survival and VEGF-A expression through its ability to activate an Akt/HIF-1α-dependent pathway. In humans, circulating CTRP3 levels are negatively correlated with several markers of systemic inflammation and cardiometabolic risk 326 .…”

Section: Cardiovascular Actions Of Select Adipokinesmentioning

confidence: 99%

See 1 more Smart Citation

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Fuster

Ouchi

Gokce

et al. 2016

Circulation Research

485

357

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Obesity is causally linked with the development of cardiovascular disorders. Accumulating evidence indicates that cardiovascular disease is the “collateral damage” of obesity-driven adipose tissue dysfunction that promotes a chronic inflammatory state within the organism. Adipose tissues secrete bioactive substances, referred to as adipokines, which largely function as modulators of inflammation. The microenvironment of adipose tissue will affect the adipokine secretome, having actions on remote tissues. Obesity typically leads to the upregulation of pro-inflammatory adipokines and the downregulation of anti-inflammatory adipokines, thereby contributing to the pathogenesis of cardiovascular diseases. In this review, we focus on the microenvironment of adipose tissue and how it influences cardiovascular disorders, including atherosclerosis and ischemic heart diseases, through the systemic actions of adipokines.

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Section: Cardiovascular Actions Of Select Adipokinesmentioning

confidence: 99%

Section: Cardiovascular Actions Of Select Adipokinesmentioning

confidence: 99%

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Fuster

Ouchi

Gokce

et al. 2016

Circulation Research

485

357

View full text Add to dashboard Cite

show abstract

“…94, 95 Additionally, CTRP6 improves cardiac function and ameliorates ventricular remodeling post-MI, protecting against cardiac fibrosis by inhibiting myofibroblast differentiation, extracellular matrix production, and cardiac fibroblast migration via Smad-independent RhoA/MRTF-A (myocardin-related transcription factor-A) signaling ( Figure 5). 96 …”

Section: Ctrp6mentioning

confidence: 99%

Role of Adipokines in Cardiovascular Disease

Lau

Ohashi

Wang

et al. 2017

Circ J

135

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Cardiovascular disease (CVD) is the greatest cause of death, accounting for nearly one-third of all deaths worldwide. The increase in obesity rates over 3 decades is widespread and threatens the public health in both developed and developing countries. Obesity, the excessive accumulation of visceral fat, causes the clustering of metabolic disorders, such as type 2 diabetes, dyslipidemia, and hypertension, culminating in the development of CVD. Adipose tissue is not only an energy storage organ, but an active endocrine tissue producing various biologically active proteins known as adipokines. Since leptin, a central regulator of food intake and energy expenditure, was demonstrated to be an adipose-specific adipokine, attention has focused on the identification and characterization of unknown adipokines to clarify the mechanisms underlying obesity-related disorders. Numerous adipokines have been identified in the past 2 decades; most adipokines are upregulated in the obese state. Adipokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and resistin are pro-inflammatory, and exacerbate various metabolic and cardiovascular diseases. However, a small number of adipokines, including adiponectin, are decreased by obesity, and generally exhibit antiinflammatory properties and protective functions against obesity-related diseases. Collectively, an imbalance in the production of pro-and antiinflammatory adipokines in the obese condition results in multiple complications. In this review, we focus on the pathophysiologic roles of adipokines with cardiovascular protective properties.

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“…Although percutaneous coronary intervention (PCI) has evidently improved the survival, post-MI heart failure still occurs after various adverse cardiac remodeling, including cardiac fibrosis, cardiomyocyte apoptosis, inflammatory reaction, etc 2 . Cardiac fibrosis, characterized by an excessive accumulation of extracellular matrix (ECM), is a process underlying cardiac remodeling post-MI 3 . Myocardium consists of cardiac fibroblasts (CFs), cardiomyocytes, smooth muscle cells, and endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway

Gao

Zhang

et al. 2017

Sci Rep

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As a newly identified factor in calcium-activated chloride channel, ANO1 participates in various physiological processes like proliferation and differentiation, and expresses in human cardiac fibroblasts. In this experiment, we investigated the function of ANO1 in cardiac fibrosis after myocardial infraction (MI) with methods of Western blotting, Quantitative real-time PCR (qRT-PCR), metabolic reduction of 3-(4,5-dimethylthiozol-2-yl)-2, 5-diphenyltetrazo-lium bromide (MTT), immunofluorescence and confocal imaging, and Masson’s trichrome staining. The results showed that the expression of ANO1 significantly increased in neonatal rats’ cardiac fibroblasts after hypoxia and in cardiac tissues after MI. After ANO1 over-expression, cardiac fibrosis was reduced in vitro and in vivo. Moreover, the expression of TGF-β and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-β/smad3 pathway in rats.

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CTRP3 attenuates post-infarct cardiac fibrosis by targeting Smad3 activation and inhibiting myofibroblast differentiation

Cited by 82 publications

References 49 publications

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Role of Adipokines in Cardiovascular Disease

ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway

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