Regulation of cardiac hypertrophy by intracellular signalling pathways

By J. Heineke, J. Molkentin. Nature reviews. Molecular cell biology, 2006

1,942 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0515914a2a925028964b5c312ca87130e65a97dd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Joseph A. Hill
2. W. Linke
3. Aik Choon Tan
4. Karen A. Ryall
5. H. Ruskoaho
6. Virpi Talman
7. P. Russell

In Molecular Biology

1. H. Ruskoaho
2. Virpi Talman
3. J. Richardson
4. Joseph A. Hill
5. Beth Levine
6. W. Linke
7. Aik Choon Tan
8. V. Veksler

Citations in the corpus

• Cardiovascular actions of insulin. (2007, background): “Thus, beneficial effects of Akt on cardiac growth may depend on temporal patterns of Akt activation as well as subcellular localization of Akt (20, 97, 104, 105).”
• Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “In pathological remodeling, the fibroblast-mediated expansion of the ECM is accompanied by the hypertrophic growth of cardiomyocytes as the cells try to compensate for the increased workload by growing in size in order to increase cardiac function and decrease ventricular wall tension (Heineke and M”
• Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. (2008, background): “35 CaN controls the expression of PGC-1 a in muscle, providing a calcium-signalling pathway whose stimulation results in increased mitochondrial content.”
• Sense and stretchability: the role of titin and titin-associated proteins in myocardial stress-sensing and mechanical dysfunction. (2007, background): “Research on mechanotransduction in normal and diseased heart is aimed at elucidating the molecular mechanisms by which myocardial structures sense physical loads and transduce them into biochemical signals to alter gene expression and modify cellular structure and function.(1) The propagation and se”
• Engineering Adolescence: Maturation of Human Pluripotent Stem Cell-derived Cardiomyocytes (2014, background): “tion will not be discussed here; for this purpose, readers may refer to the excellent review by Heineke and Molkentin.(76)”
• Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. (2009, background): “Whereas HATs, such as p300 and PCAF, are prohypertrophic, HDACs of different classes have been shown to have different effects on cardiac growth, resulting from stress stimuli (1, 3).”
• Cardiac autophagy is a maladaptive response to hemodynamic stress. (2007, background): “Numerous signaling pathways have been causally implicated in stress-induced remodeling of the heart (2, 3), and many of these same pathways have also been implicated in cell death.”
• Cell and Molecular Biology (2009, background): “The two other major signaling pathways which are important for the mediation of physiological cardiac hypertrophy are the Ras-extracellular signal-regulated kinase-mitogen activated protein kinase (Erk-MAPK) and the phosphatidylinositol 30-kinase (PI3K)–Akt1 pathways (Heinke and Molkentin, 2006).”
• Systems biology approaches for advancing the discovery of effective drug combinations (2015, background): “Pharmaceutical research has increasingly relied on re-ductionist approaches, even though systemic diseases such as cancer and heart disease are managed by large, interconnected networks with many pathways affecting pathological signaling [4,5].”