Cardiac hypertrophy: the good, the bad, and the ugly.

By Norbert Frey, E. Olson. Annual Review of Physiology, 2003

1,535 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b06895f1df2e4ca775d7d255defa733ad46db70b

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. E. Olson
2. Joseph A. Hill
3. W. Linke
4. S. Offermanns
5. Yibin Wang
6. N. Wettschureck
7. T. Force

In Molecular Biology

1. E. Olson
2. J. Richardson
3. Joseph A. Hill
4. W. Linke
5. T. McKinsey
6. Yibin Wang
7. Chun-li Zhang
8. S. Offermanns

Citations in the corpus

• Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development (2004, background): “It should be noted in this regard that many forms of cardiac stress are accompanied by the activation of complex neurohumoral signals that act through interconnected signaling pathways (2, 8, 22, 34).”
• Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “Most importantly, the signaling mechanisms mediating the critical transition from compensated hypertrophy to decompensated heart failure remain poorly understood (104, 133, 369).”
• Role of oxidative stress in cardiac hypertrophy and remodeling. (2007, background): “of reactive oxygen species and NAD(P)H oxidase in alpha(1)-”
• Mammalian G proteins and their cell type specific functions. (2005, background): “Such pathological myocardial hypertrophy was shown to be associated with increased cardiac mortality (191, 285, 535), raising the question whether prevention of pathological hypertrophy is beneficial or not (191).”
• Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy (2005, background): “This response involves the stimulation of multiple signaling and transcription pathways that induce hypertrophic remodelin”
• Sense and stretchability: the role of titin and titin-associated proteins in myocardial stress-sensing and mechanical dysfunction. (2007, background): “transduce them into biochemical signals to alter gene expression and modify cellular structure and function (Frey and Olson, 2003; Heineke and Molkentin, 2006; Olson, 2006).”