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Open AccessJournal ArticleDOI

A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy

TLDR
It is shown that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus.
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This article is published in Cell.The article was published on 1998-04-17 and is currently open access. It has received 2596 citations till now. The article focuses on the topics: NFAT Pathway & Calcineurin.

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Citations
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Calcium signalling: dynamics, homeostasis and remodelling

TL;DR: The Ca2+-signalling toolkit is used to assemble signalling systems with very different spatial and temporal dynamics and has a direct role in controlling the expression patterns of its signalling systems that are constantly being remodelled in both health and disease.
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Mammalian Mitogen-Activated Protein Kinase Signal Transduction Pathways Activated by Stress and Inflammation

TL;DR: This review focuses on the biochemical components and regulation of mammalian stress-regulated mitogen-activated protein kinase (MAPK) pathways, and the nuclear factor-kappa B pathway, a second stress signaling paradigm.
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Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.

TL;DR: It is concluded that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of this pathway can oppose muscle atrophy induced by disuse.
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Transcriptional regulation by calcium, calcineurin, and NFAT

TL;DR: The NFAT family of transcription factors encompasses five proteins evolutionarily related to the Rel/NF B family, and it is clear that NFAT activates transcription of a large number of genes during an effective immune response.
Journal ArticleDOI

Regulation of cardiac hypertrophy by intracellular signalling pathways

TL;DR: Recent findings in genetically modified animal models implicate important intermediate signal-transduction pathways in the coordination of heart growth following physiological and pathological stimulation.
References
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TRANSCRIPTION FACTORS OF THE NFAT FAMILY:Regulation and Function

TL;DR: Recent data on the diversity of the NFAT family of transcription factors, the regulation of NFAT proteins within cells, and the cooperation ofNFAT proteins with other transcription factors to regulate the expression of inducible genes are discussed.
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Differential activation of transcription factors induced by Ca2+ response amplitude and duration

TL;DR: It is reported here that the amplitude and duration of calcium signals in B lymphocytes controls differential activation of the pro–inflammatory transcriptional regulators NF-κB, c-Jun N-terminal kinase (JNK) and NFAT, revealing a mechanism by which a multifunctional second messenger such as Ca2+ can achieve specificity in signalling to the nucleus.
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Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro

TL;DR: Using an in vitro model of load (stretch)-induced cardiac hypertrophy, it is demonstrated that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response.
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Nuclear association of a T-cell transcription factor blocked by FK-506 and cyclosporin A.

TL;DR: NF-AT is formed when a signal from the antigen receptor induces a pre-existing cytoplasmic subunit to translocate to the nucleus and combine with a newly synthesized nuclear subunit of NF-AT, forming a inhibitory complex between the drug and isomerase.
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The cellular and molecular response of cardiac myocytes to mechanical stress

TL;DR: Various cell signaling mechanisms initiated by mechanical stress on cardiac myocytes are summarized with emphasis on potential mechanosensing mechanisms and the relationship between mechanical loading and the cardiac renin-angiotensin system.
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