Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Jianming Jiang"'
Autor:
Weiming Chen, Jianming Jiang, Roger Foo, Jin-Song Bian, Dan Liao, Ida G. Lunde, Christine E. Seidman, Matthew Ackers-Johnson, Jonathan G. Seidman, Feng Zhu, Pui Shi Chan, Jiong-Wei Wang, Jing Xuan Wong, Qidong Hu, Lek Wen Tan, Hiroko Wakimoto, Hansen Tan, Chia Yee Tan
Publikováno v:
Circulation Research. 125:834-846
Rationale: Pathogenic variations in the lamin gene ( LMNA ) cause familial dilated cardiomyopathy (DCM). LMNA insufficiency caused by LMNA pathogenic variants is believed to be the basic mechanism underpinning LMNA -related DCM. Objective: To assess
Autor:
Roger Foo, Cheryl Xueli Chan, Dominic Paul Lee, Xingfan Huang, Chang Jie Mick Lee, Sarah Ng, Melissa J. Fullwood, Motakis Efthymios, Erez Lieberman Aiden, Zenia Tiang, Shyam Prabhakar, Wen Tan Wl, Chukwuemeka George Anene-Nzelu, Matias I. Autio, Tuan Danh Anh Luu, Jianming Jiang, Peter Yiqing Li
Publikováno v:
Circulation. 139:1937-1956
Background: The human genome folds in 3 dimensions to form thousands of chromatin loops inside the nucleus, encasing genes and cis -regulatory elements for accurate gene expression control. Physical tethers of loops are anchored by the DNA-binding pr
Autor:
Chia Yee Tan, Jianming Jiang
Publikováno v:
Circulation Research. 127
Introduction: The mammalian hearts including humans have a limited regenerative capacity. Activation of proliferation or related signaling pathways has been shown to reinstate cell renewal capacity of cardiomyocytes (CM) which is believed to ameliora
Autor:
Jianming Jiang, Chia Yee Tan
Publikováno v:
Circulation Research. 125
Introduction: Cardiac Lmna insufficiency causes dilated cardiomyopathy (DCM) coupled with cardiac fibrosis and inflammation. TGFβ family members are key mediators for cardiac performance, cardiac fibrosis and inflammation. However, how TGFβ family
Autor:
Christopher N Toepfer, Hiroko Wakimoto, Amanda C Garfinkel, Barbara McDonough, Dan Liao, Jianming Jiang, Angela Tai, Josh Gorham, Ida G Lund, Mingyue Lun, Thomas L Lynch, Sakthivel Sadayappan, Charles S Redwood, Hugh Watkins, Jonathan Seidman, Christine Seidman
Publikováno v:
Circulation Research. 123
The mechanisms by which truncating mutations in MYBPC3 (encoding cardiac myosin binding protein-C; cMyBPC) or myosin missense mutations cause hyper-contractility and poor relaxation in hypertrophic cardiomyopathy (HCM) are incompletely understood. Us
Autor:
Yangtai Guan, Ying Han, Xiaohua Wu, Jie-Ning Wang, Zhiliang Yu, Jianming Jiang, Huijun Xie, Yong Qin
Publikováno v:
Journal of Cardiovascular Pharmacology and Therapeutics. 20:563-571
Basilar vascular smooth muscle cells (BASMCs) hyperplasia is a prominent feature of cerebrovascular remodeling and stroke during the development of hypertension. Tanshinone IIA (Tan) has been reported to exhibit a protective effect against the pathol
Autor:
Michael A. Burke, Joshua M. Gorham, Christine E. Seidman, Steve Depalma, Ju Chen, Jonathan G. Seidman, Daniel M. DeLaughter, Srinivasan Mukundan, Anna Axelsson, Danos C. Christodoulou, Michael Jerosch-Herold, Ilton M Cubero Salazar, Hiroko Wakimoto, Jianming Jiang, Craig C. Benson
Publikováno v:
Circulation Research. 117
Four-and-a-half-LIM-domain protein-1 (FHL1) participates in the heart’s response to biomechanical stress during pathological states. Normally, the basal isoform, bFhl1 , predominates in non-stressed states. In pathology, a change in start site lead
Autor:
Zhiqiang Lin, Alexander von Gise, Pingzhu Zhou, Qing Ma, Jinghai Chen, Jianming Jiang, Jonathan G Seidman, Da-zhi Wang, William T Pu
Publikováno v:
Circulation Research. 115
Background: Yes-Associated Protein (YAP), the terminal effector of the Hippo signaling pathway, is crucial for regulating embryonic cardiomyocyte proliferation. We hypothesized that YAP activation after myocardial infarction would preserve cardiac fu
Autor:
Jianming Jiang, Hiroko Wakimoto, Kenji Onoue, Gregory M Fomovsky, Richard T Lee, Jonathan G Seidman, Christine E Seidman
Publikováno v:
Circulation Research. 113
Introduction: Wildtype neonatal murine cardiomyocytes become bi-nucleated, hypertrophy and terminally differentiate, and concurrently develop well-organized striation patterns of sarcomeres of myofibrils. Neonatal mice lacking cardiac myosin binding
Autor:
Gregory M Fomovsky, Richard T. Lee, Hesham A. Sadek, Jonathan G. Seidman, Kimberly K Schaefer, Christine E. Seidman, Joseph Gannon, Hiroko Wakimoto, Jianming Jiang
Publikováno v:
Circulation Research. 113
Introduction: Adult mammalian cardiac regeneration rate is inadequate to compensate for the loss of myocardium following injury. One-day old (P1) mice fully regenerate myocardium after ventricular apex resection by division of cardiomyocytes (CMs). T