Regulatory mechanism of gallic acid against advanced glycation end products induced cardiac remodeling in experimental rats

Umadevi, S.; Gopi, Venkatachalam; Vellaichamy, Elangovan

doi:10.1016/j.cbi.2013.11.013

Cited by 65 publications

(37 citation statements)

References 46 publications

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“…Despite little being known about the molecular mechanism linking AGEs to fibrosis, there is evidence supporting that TGF- β may play a major role [66]. Furthermore, in addition to stimulation of fibroblast proliferation and deposition of types I and III collagen, AGEs contribute to enhancement of ECM accumulation, compromising the heart's diastolic function [67, 68]. …”

Section: Myocardial Fibrosismentioning

confidence: 99%

A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

Schirone

Forte

Palmerio

et al. 2017

Oxidative Medicine and Cellular Longevity

338

241

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Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.

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Section: Myocardial Fibrosismentioning

confidence: 99%

A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

Schirone

Forte

Palmerio

et al. 2017

Oxidative Medicine and Cellular Longevity

338

241

View full text Add to dashboard Cite

show abstract

“…We studied the effects of the loss of CTSB function via the production of CTSB-KO mice and showed that CTSB deficiency results in attenuated cardiac hypertrophy, fibrosis, and better preservation of cardiac function following pressure overload, strongly suggesting that CTSB is an essential regulator of cardiac remodeling (34). We noticed that the end-systolic pressure was significant different between sham WT and sham KO mice in Table 1, while others were not significantly different.…”

mentioning

confidence: 90%

Cathepsin B deficiency attenuates cardiac remodeling in response to pressure overload via TNF-α/ASK1/JNK pathway

Yuan

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Cathepsin B (CTSB), a member of the lysosomal cathepsin family that is expressed in both murine and human hearts, was previously shown to participate in apoptosis, autophagy, and the progression of certain types of cancers. Recently, CTSB has been linked to myocardial infarction. Given that cathepsin L, another member of the lysosomal cathepsin family, ameliorates pathological cardiac hypertrophy, we hypothesized that CTSB plays a role in pressure overload-induced cardiac remodeling. Here we report that CTSB was upregulated in cardiomyocytes in response to hypertrophic stimuli both in vivo and in vitro. Moreover, knockout of CTSB attenuated pressure overload-induced cardiac hypertrophy, fibrosis, dysfunction, and apoptosis. Furthermore, the aortic banding-induced activation of TNF-α, apoptosis signal-regulating kinase 1 (ASK1), c-Jun NH2-terminal kinases (JNK), c-Jun, and release of cytochrome c was blunted by CTSB deficiency, which was further confirmed in in vitro studies induced by angiotensin II. In cardiomyocytes pretreatment with SP600125, a JNK inhibitor, suppressed the cardiomyocytes hypertrophy by inhibiting the ASK1/JNK pathway. Altogether, these data indicate that the CTSB protein functions as a necessary modulator of hypertrophic response by regulating TNF-α/ASK1/JNK signaling pathway involved in cardiac remodeling.

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“…So far, the antidiabetic and even antiglycative effects of kaempferol, ferulic acid and/or gallic acid have been reported [31][32][33][34]. Therefore, it seems highly possible that these compounds presented in this extract of H. cordata leaves executed the observed antidiabetic protection.…”

Section: Discussionmentioning

confidence: 88%

Houttuynia cordata aqueous extract attenuated glycative and oxidative stress in heart and kidney of diabetic mice

Hsu

Yang

et al. 2015

Eur J Nutr

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Regulatory mechanism of gallic acid against advanced glycation end products induced cardiac remodeling in experimental rats

Cited by 65 publications

References 46 publications

A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

Cathepsin B deficiency attenuates cardiac remodeling in response to pressure overload via TNF-α/ASK1/JNK pathway

Houttuynia cordata aqueous extract attenuated glycative and oxidative stress in heart and kidney of diabetic mice

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