Myocardial Cell Death and Regeneration during Progression of Cardiac Hypertrophy to Heart Failure
Sagartirtha Sarkar,Mamta Chawla-Sarkar,David Young,Kazutoshi Nishiyama,Mary E. Rayborn,Joe G. Hollyfield,Subha Sen +6 more
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TLDR
It is demonstrated, for the first time in an animal model, that cell death and regeneration occur simultaneously in myocytes during end-stage heart failure, a phenomenon not observed at the onset of the disease process.About:
This article is published in Journal of Biological Chemistry.The article was published on 2004-12-10 and is currently open access. It has received 39 citations till now. The article focuses on the topics: Heart failure & Muscle hypertrophy.read more
Citations
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Cardiovascular disease models: A game changing paradigm in drug discovery and screening
Houman Savoji,Houman Savoji,Mohammad Hossein Mohammadi,Mohammad Hossein Mohammadi,Naimeh Rafatian,Masood Khaksar Toroghi,Erika Yan Wang,Yimu Zhao,Anastasia Korolj,Samad Ahadian,Milica Radisic,Milica Radisic +11 more
TL;DR: Current in vitro, in vivo, and in silico platforms for modelling healthy and pathological cardiac tissues and their advantages and disadvantages for drug screening and discovery applications are described and a roadmap for employing these non-animal platforms in assessing drug cardiotoxicity and safety is suggested.
Journal ArticleDOI
Inhibition of signal transducer and activator of transcription 3 (STAT3) attenuates interleukin-6 (IL-6)-induced collagen synthesis and resultant hypertrophy in rat heart.
Saiful A. Mir,Arunachal Chatterjee,Arkadeep Mitra,Kanchan Pathak,Sushil K. Mahata,Sagartirtha Sarkar +5 more
TL;DR: Compared with IL-6 neutralization, more pronounced down-regulation of collagen synthesis and regression ofhypertrophy was observed with STAT3 inhibition, suggesting that STAT3 is the major downstream signaling molecule and a potential therapeutic target for cardiac hypertrophy.
Journal Article
Small mammalian animal models of heart disease.
TL;DR: This review presents a guideline for the commonly used small animal models used in cardiac research as an effort to standardize the most relevant procedures and obtain translatable and reproducible results.
Journal ArticleDOI
Role of α-crystallin B as a regulatory switch in modulating cardiomyocyte apoptosis by mitochondria or endoplasmic reticulum during cardiac hypertrophy and myocardial infarction
Arkadeep Mitra,Trayambak Basak,Kaberi Datta,Shaon Naskar,Shantanu Sengupta,Sagartirtha Sarkar +5 more
TL;DR: The study demonstrated for the first time that two different organelles—mitochondria and ER have predominant roles in mediating cardiomyocyte death signaling during hypertrophy and MI, respectively, and activation of CRYAB acts as a molecular switch in bypassing mitochondrial pathway of apoptosis during MI.
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Ubiquitination and Degradation of the Anti-apoptotic Protein ARC by MDM2
TL;DR: It is concluded that MDM2 is a critical regulator of ARC levels in cardiomyocytes and prevention ofMDM2-induced degradation of ARC represents a potential therapeutic target to preventCardiomyocyte apoptosis.
References
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Adult Cardiac Stem Cells Are Multipotent and Support Myocardial Regeneration
Antonio Paolo Beltrami,Laura Barlucchi,Daniele Torella,Mathue Baker,Federica Limana,Stefano Chimenti,Hideko Kasahara,Marcello Rota,Ezio Musso,Konrad Urbanek,Annarosa Leri,Jan Kajstura,Bernardo Nadal-Ginard,Piero Anversa +13 more
TL;DR: The existence of Lin(-) c-kit(POS) cells with the properties of cardiac stem cells, which are self-renewing, clonogenic, and multipotent, giving rise to myocytes, smooth muscle, and endothelial cells are reported.
Journal ArticleDOI
Bcl-2 functions in an antioxidant pathway to prevent apoptosis
TL;DR: A model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation is proposed in which it protected cells from H2O2- and menadione-induced oxidative deaths and suppressed lipid peroxidation completely.
Journal ArticleDOI
Principles of CDK regulation
TL;DR: The activity of cyclin-dependent kinases is controlled by four highly conserved biochemical mechanisms, forming a web of regulatory pathways unmatched in its elegance and intricacy.
Journal ArticleDOI
Induction of apoptosis in fibroblasts by c-myc protein
Gerard I. Evan,Andrew H. Wyllie,Christopher S. Gilbert,Trevor Littlewood,Hartmut Land,Mary W. Brooks,Catherine M. Waters,Linda Z. Penn,David C. Hancock +8 more
TL;DR: It is demonstrated that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.
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