Cardiac Hypertrophy: Molecular and Cellular Events

Carreño, Juan; Apablaza, Felipe; Ocaranza, María Paz; Jalil, Jorge

doi:10.1016/s1885-5857(06)60796-2

Cited by 60 publications

(58 citation statements)

References 143 publications

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“…Cardiac hypertrophy is characterized by the abnormal enlargement of cardiomyocytes, originating from an increase in myocyte size and the proliferation of non-muscle cells (13). Numerous clinical studies have indicated that sustained cardiac hypertrophy is a maladaptive process, ultimately leading to decompensated heart failure (14).…”

Section: B a D Cmentioning

confidence: 99%

Naringenin attenuates pressure overload-induced cardiac hypertrophy

Zhang

Zheng

Yuan

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Cardiac hypertrophy is characterized by abnormal enlargement of cardiomyocytes and disproportionate accumulation of extracellular interstitial fibrosis, which are major predictors of the development of coronary artery disease and heart failure. Naringenin is a bitter principle component of grapefruit that has numerous pharmacological effects, including anti-inflammatory, hypolipidemic, antithrombotic and antiatherogenic properties. In order to investigate whether naringenin is able to exert a protective effect against cardiac hypertrophy induced by pressure overload, aortic banding (AB) was performed to induce cardiac hypertrophy in mice, and naringenin was administered for 7 weeks. A total of 60 mice were allocated into four groups: Sham + vehicle, AB + vehicle, sham + naringenin and AB + naringenin. Naringenin treatment attenuated cardiac dysfunction, as indicated by the results of echocardiography and catheter-based measurements at 8 weeks post-surgery. The extent of cardiac hypertrophy was assessed by the heart weight/body weight, heart weight/tibial length and lung weight/body weight ratios, in addition to the cardiomyocyte cross-sectional area and the mRNA expression levels of hypertrophic maker, all of which were mitigated by naringenin administration. Naringenin also inhibited the expression of transforming growth factor-β1, connective tissue growth factor, collagen Iα and collagen IIIα, and attenuated interstitial fibrosis. In addition, naringenin downregulated the activation of the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathways. In conclusion, naringenin attenuated cardiac hypertrophy and interstitial fibrosis, in addition to improving left ventricular function in pressure-overloaded mice. The cardioprotective effect exerted by naringenin may be associated with the inhibition of PI3K/Akt, ERK and JNK signaling pathways.

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Section: B a D Cmentioning

confidence: 99%

Naringenin attenuates pressure overload-induced cardiac hypertrophy

Zhang

Zheng

Yuan

et al. 2015

Experimental and Therapeutic Medicine

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“…Features of cardiac hypertrophy include increased cardiomyocyte size, protein synthesis, elevated fetal gene atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), β-myosin heavy chain (β-MHC) and fibronectin protein expression, and abnormal sarcomeric organization. Cell signaling pathways involved in cardiac hypertrophy include mitogen-activated protein kinase (MAPK), adenosine monophosphate-activated protein kinase (AMPK), transforming growth factor β (TGF-β)/smads, Ras/Rho, janus kinase (JAK)/signal transducers and activators of transcription (STAT), and calcinurin/nuclear factor of activated T-cells (NFAT) (1,2).…”

Section: Introductionmentioning

confidence: 99%

LKB1/AMPK pathway mediates resistin-induced cardiomyocyte hypertrophy in H9c2 embryonic rat cardiomyocytes

Liu

Cheng

et al. 2016

Biomedical Reports

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Abstract.Resistin has been previously demonstrated to induce cardiac hypertrophy, however, the underlying molecular mechanisms of resistin-induced cardiac hypertrophy remain unclear. Using H9c2 cells, the present study investigated the liver kinase B1 (LKB1)/adenosine monophosphate-activated protein kinase (AMPK) signaling pathway for a potential role in mediating resistin-induced cardiomyocyte hypertrophy. Treatment of H9c2 cells with resistin increased cell surface area, protein synthesis, and expression of hypertrophic marker brain natriuretic peptide and β-myosin heavy chain. Treatment with metformine attenuated these effects of resistin. Furthermore, treatment with resistin decreased phosphorylation of LKB1 and AMPK, whereas pretreatment with metformin increased phosphorylation of LKB1 and AMPK that is reduced by resistin. These results suggest that resistin induces cardiac hypertrophy through the inactivation of the LKB1/AMPK cell signaling pathway.

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“…Despite advances made in heart research over the past two decades, heart disease remains the leading cause of death in North America and accounts for about 45% of all deaths [2]. Cardiac hypertrophy (enlargement of the heart) is an adaptive response of the heart to pressure and/or volume overload [3]. However, prolonged hypertrophy is a well-known risk factor for cardiovascular mortality [4,5].…”

Section: Introductionmentioning

confidence: 99%