نتایج جستجو برای: nuclear hypertrophy

تعداد نتایج: 279538  

Journal: :iranian journal of public health 0
m. mirdamadi m. golshan b. aflaki h. nazemian m. salimi

a prospective study of 550 consecutive mothers delivered in amin ob. gyn center of isfahan university was performed to determine the relationships between maternal anemia, placental weight and neonatal birth weight. the important findings were marked placental hypertrophy in anemic mothers. (r= -/9.95) .it is probable that in anemic mothers placental hypertrophy is a compensatory mechanism resp...

2012
Chao-Sheng Lo Shiao-Ying Chang Isabelle Chenier Janos G. Filep Julie R. Ingelfinger Shao Ling Zhang John S.D. Chan

We investigated the impact of heterogeneous nuclear ribonucleoprotein F (hnRNP F) overexpression on angiotensinogen (Agt) gene expression, hypertension, and renal proximal tubular cell (RPTC) injury in high-glucose milieu both in vivo and in vitro. Diabetic Akita transgenic (Tg) mice specifically overexpressing hnRNP F in their RPTCs were created, and the effects on systemic hypertension, Agt g...

2015
Nouf M Al-rasheed Maha M Al-Oteibi Reem Z Al-Manee Sarah A Al-shareef Nawal M Al-Rasheed Iman H Hasan Raeesa A Mohamad Ayman M Mahmoud

Simvastatin (SIM) is a lipid-soluble inhibitor of hydroxy-3-methylglutaryl coenzyme A reductase with multiple reported therapeutic benefits. The present study was designed to investigate the effect of pretreatment with SIM on isoproterenol (ISO)-induced cardiac hypertrophy in rats. Twenty-four male albino Wistar rats weighing 180-200 g were divided into four groups. Groups I and III received no...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2001
L A Leinwand

T heart is remarkably plastic, changing its size, shape, and function in response to a wide variety of stimuli. Beyond birth, by far the greatest cardiac growth occurs by cellular hypertrophy, rather than hyperplasia. When normal cardiac size has been reached, additional changes in size can occur in response to stimuli such as hypertension, defective genes, or exercise, to name a few. Although ...

Journal: :Circulation 2015
Malik Bisserier Magali Berthouze-Duquesnes Magali Breckler Florence Tortosa Loubina Fazal Annélie de Régibus Anne-Coline Laurent Audrey Varin Alexandre Lucas Maxime Branchereau Pauline Marck Jean-Nicolas Schickel Claudine Deloménie Olivier Cazorla Pauline Soulas-Sprauel Bertrand Crozatier Eric Morel Christophe Heymes Frank Lezoualc'h

BACKGROUND Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and is regulated by various signaling pathways. However, the molecular mechanisms that negatively regulate these signal transduction pathways remain poorly understood. METHODS AND RESULTS Here, we characterized Carabin, a protein expressed in cardiomyocytes that was downregulated in cardiac hypertr...

2017
Xiao-Hui Guan Xuan Hong Ning Zhao Xiao-Hong Liu Yun-Fei Xiao Ting-Tao Chen Li-Bin Deng Xiao-Lei Wang Jian-Bin Wang Guang-Ju Ji Mingui Fu Ke-Yu Deng Hong-Bo Xin

Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2 O2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart...

2017
Tsung-Ming Lee Shinn-Zong Lin Nen-Chung Chang

Activation of phosphoinositide 3-kinase (PI3K)/Akt signalling is the molecular pathway driving physiological hypertrophy. As lithium, a PI3K agonist, is highly toxic at regular doses, we assessed the effect of lithium at a lower dose on ventricular hypertrophy after myocardial infarction (MI). Male Wistar rats after induction of MI were randomized to either vehicle or lithium (1 mmol/kg per day...

Journal: :Circulation. Heart failure 2014
Yasuhiro Maejima Soichiro Usui Peiyong Zhai Masayuki Takamura Shuichi Kaneko Daniela Zablocki Mitsuhiro Yokota Mitsuaki Isobe Junichi Sadoshima

BACKGROUND Muscle-specific RING finger protein-1 (MuRF1) is an E3 ligase that inhibits cardiac hypertrophy. However, how MuRF1 regulates cardiac hypertrophy and function during pressure overload (PO) remains poorly understood. We investigated the role of endogenous MuRF1 in regulating cardiac hypertrophy in response to PO in vivo. METHODS AND RESULTS Transverse aortic constriction (TAC) for 4...

Journal: :International Journal of Biological Sciences 2008
Christopher D. Willey Arun P. Palanisamy Rebecca K. Johnston Santhosh K. Mani Hirokazu Shiraishi William J. Tuxworth Michael R. Zile Sundaravadivel Balasubramanian Dhandapani Kuppuswamy

Growth, survival and cytoskeletal rearrangement of cardiomyocytes are critical for cardiac hypertrophy. Signal transducer and activator of transcription-3 (STAT3) activation is an important cardioprotective factor associated with cardiac hypertrophy. Although STAT3 activation has been reported via signaling through Janus Kinase 2 (JAK2) in several cardiac models of hypertrophy, the importance o...

Journal: :Cardiovascular research 2010
Biswajit Das David Young Amit Vasanji Sudhiranjan Gupta Sagartirtha Sarkar Subha Sen

AIMS Cardiac-specific overexpression of myotrophin (myo) protein in transgenic (myo-Tg) mice results in hypertrophy at 4 weeks that progresses to heart failure (HF) by 36 weeks. Gene profiling showed that p53 expression increases as hypertrophy worsens to HF, suggesting that p53 may influence myo-induced HF. We aimed to define how the p53 signalling cascade affects the spectrum of cardiac hyper...

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