Cardiomegaly

Publication Title: 
Journal of the American Geriatrics Society
Author(s): 
Berman, B. H.
Leon, D. F.
Publication Title: 
The Tohoku Journal of Experimental Medicine

Myocardial infarction (MI) leads to progressive left ventricular (LV) dilatation and is associated with interstitial fibrosis in the non-infarcted myocardium. The NF-?B signaling pathway plays an important role in ventricular remodeling after MI. Recent studies have indicated that the anti-malarial agent artemisinin can inhibit NF-?B activation, which may attenuate post-infarct myocardial remodeling. In this study, we investigated the effect of artemisinin on post-infarct myocardial remodeling using a rat model of MI.

Author(s): 
Gu, Yongwei
Wang, Xi
Wang, Xin
Yuan, Mingjie
Wu, Gang
Hu, Juan
Tang, Yanhong
Huang, Congxin
Publication Title: 
Diabetes, Obesity & Metabolism

AIMS: We investigated the effect of the water extract of Salacia oblonga (SOE), an ayurvedic antidiabetic and antiobesity medicine, on obesity and diabetes-associated cardiac hypertrophy and discuss the role of modulation of cardiac angiotensin II type 1 receptor (AT(1)) expression in the effect. METHODS: SOE (100 mg/kg) was given orally to male Zucker diabetic fatty (ZDF) rats for 7 weeks. At the end-point of the treatment, the hearts and left ventricles were weighed, cardiomyocyte cross-sectional areas were measured, and cardiac gene profiles were analysed.

Author(s): 
Huang, T. H.
He, L.
Qin, Q.
Yang, Q.
Peng, G.
Harada, M.
Qi, Y.
Yamahara, J.
Roufogalis, B. D.
Li, Y.
Publication Title: 
Journal of Cardiovascular Pharmacology

Cardiac hypertrophy occurs in response to increased workload, such as hypertension or valvular heart disease. Oxidative stress has been implicated in cardiac hypertrophy and in its transition to heart failure. This study was taken up with the objective to evaluate the role of oxidative stress in cardiomyoblast hypertrophy and its modulation by Desmodium gangeticum (DG) that has been traditionally used in Ayurveda, an Indian system of medicine. The methanolic root extract was analyzed for total phenolic content and tested for antioxidant potential.

Author(s): 
Sankar, Vandana
Pangayarselvi, Balasubramaniam
Prathapan, Ayyappan
Raghu, Kozhiparambil Gopalan
Publication Title: 
American Journal of Physiology. Heart and Circulatory Physiology

In the present study, we examined whether NF-kappaB activation is required for cardiac hypertrophy in vivo. Cardiac hypertrophy in rats was induced by aortic banding for 1, 3, and 5 days and 1-6 wk, and age-matched sham-operated rats served as controls. In a separate group of rats, an IkappaB-alpha dominant negative mutant (IkappaB-alphaM), a superrepressor of NF-kappaB activation, or pyrrolidinedithiocarbamate (PDTC), an antioxidant that can inhibit NF-kappaB activation, was administered to aortic-banded rats for 3 wk.

Author(s): 
Li, Yuehua
Ha, Tuanzhu
Gao, Xiang
Kelley, Jim
Williams, David L.
Browder, I. William
Kao, Race L.
Li, Chuanfu
Publication Title: 
Cardiovascular Research

OBJECTIVE: We have previously demonstrated that nuclear factor kappa B (NFkappaB) activation is needed for the development of cardiac hypertrophy in vivo. NFkappaB is a downstream transcription factor in the Toll-like receptor (TLR)-mediated signaling pathway; therefore, we investigated a role of TLR4 in cardiac hypertrophy in vivo. METHODS: TLR4-deficient mice (C.C3H-Tlr4(lps-d), n = 6), wild-type (WT) genetic background mice (BALB/c, n = 6), TLR4-deleted strain (C57BL/10ScCr, n = 8), and WT controls (C57BL/10ScSn, n = 8) were subjected to aortic banding for 2 weeks.

Author(s): 
Ha, Tuanzhu
Li, Yuehua
Hua, Fang
Ma, Jinag
Gao, Xiang
Kelley, Jim
Zhao, Aiqiu
Haddad, Georges E.
Williams, David L.
William Browder, I.
Kao, Race L.
Li, Chuanfu
Publication Title: 
American Journal of Physiology. Heart and Circulatory Physiology

In this study, we evaluated whether blocking myeloid differentiation factor-88 (MyD88) could decrease cardiac myocyte apoptosis following pressure overload. Adenovirus expressing dominant negative MyD88 (Ad5-dnMyD88) or Ad5-green fluorescent protein (GFP) (Ad5-GFP) was transfected into rat hearts (n = 8/group) immediately followed by aortic banding for 3 wk. One group of rats (n = 8) was subjected to aortic banding for 3 wk without transfection. Sham surgical operation (n = 8) served as control.

Author(s): 
Ha, Tuanzhu
Hua, Fang
Li, Yuehua
Ma, Jing
Gao, Xiang
Kelley, Jim
Zhao, Aiqiu
Haddad, Georges E.
Williams, David L.
Browder, I. William
Kao, Race L.
Li, Chuanfu
Publication Title: 
Cardiovascular Research

AIMS: Nuclear factor-kappaB (NF-kappaB) plays a critical role in cell growth and inflammation during the progression of cardiac hypertrophy and heart failure. Several members of nuclear receptor superfamily, including liver X receptors (LXRalpha and LXRbeta), have been shown to suppress inflammatory responses, but little is known about their effects in cardiomyocytes. METHODS AND RESULTS: We investigated LXR expression patterns in pressure overload-induced hypertrophic hearts and the hypertrophic growth of the LXRalpha-deficient hearts from mice (C57/B6) in response to pressure overload.

Author(s): 
Wu, Sijie
Yin, Ran
Ernest, Rick
Li, Yuquan
Zhelyabovska, Olga
Luo, Jinwen
Yang, Yifeng
Yang, Qinglin
Publication Title: 
Laboratory Investigation; a Journal of Technical Methods and Pathology

Cardiac hypertrophy is a common finding in human patients with inborn errors of long-chain fatty acid oxidation. Mice with either very long-chain acyl-coenzyme A dehydrogenase deficiency (VLCAD-/-) or long-chain acyl-coenzyme A dehydrogenase deficiency (LCAD-/-) develop cardiac hypertrophy. Cardiac hypertrophy, initially measured using heart/body weight ratios, was manifested most severely in LCAD-/- male mice. VLCAD-/- mice, as a group, showed a mild increase in normalized cardiac mass (8.8% hypertrophy compared with all wild-type (WT) mice).

Author(s): 
Cox, Keith B.
Liu, Jian
Tian, Liqun
Barnes, Stephen
Yang, Qinglin
Wood, Philip A.
Publication Title: 
Circulation Research

RATIONALE: Peroxisome proliferator-activated receptors (PPARs) (alpha, gamma, and delta/beta) are nuclear hormone receptors and ligand-activated transcription factors that serve as key determinants of myocardial fatty acid metabolism. Long-term cardiomyocyte-restricted PPARdelta deficiency in mice leads to depressed myocardial fatty acid oxidation, bioenergetics, and premature death with lipotoxic cardiomyopathy. OBJECTIVE: To explore the essential role of PPARdelta in the adult heart.

Author(s): 
Wang, Peiyong
Liu, Jian
Li, Yuquan
Wu, Sijie
Luo, Jinwen
Yang, Huan
Subbiah, Ramasamy
Chatham, John
Zhelyabovska, Olga
Yang, Qinglin

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