The conserved phosphoinositide 3‐kinase pathway determines heart size in mice

By T. Shioi, P. Kang, P. Douglas, J. Hampe, C. Yballe, J. Lawitts, Lewis C. Cantley, S. Izumo. EMBO Journal, 2000

637 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Ecology, Epidemiology

View Paper: https://www.semanticscholar.org/paper/718952afde5c86e117085296a6dfc5ebc18c3e03

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. T. Force
2. J. Molkentin
3. J. Heineke
4. Nahum Sonenberg
5. K. Weeks
6. Bianca C. Bernardo
7. J. McMullen

In Epidemiology

1. K. Guan
2. M. Wymann
3. Jun Wu
4. Nahum Sonenberg
5. T. P. Neufeld
6. K. Inoki
7. T. Force
8. I. Slaninová

Citations in the corpus

• The phosphatidylinositol 3-Kinase–AKT pathway in human cancer (2002, background): “The p110α mice develop large hearts owing to increased cell size (growth) without affecting cell number or apoptosis, whereas the expression of dominant-negative p110α gives a small-heart phenotyp”
• TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling (2002, background): “In mice, overexpression of constitutively active PI(3)K or Akt in the heart results in hypertroph”
• Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “Changes in heart size were due to changes in myocyte size rather than number (Shioi et al., 2000).”
• Regulation of translation initiation by FRAP/mTOR. (2001, background): “PI3K signaling regulates cell and organ size of the mouse heart (Shioi et al. 2000).”
• Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “With respect to the regulation of cardiac hypertrophy, the expression of constitutively active p110α in the heart produced a form of physiological cardiac hypertrophy with preserved ventricular function (up to one year of age”
• Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “2010), the majority of data indicate that IGF1R, PI3K (p110α) and Akt1 play critical roles in the induction of adaptive physiological heart growth (DeBosch et al. 2006; Kim et al. 2008; Luo et al. 2005; McMullen et al. 2003, 2004; Shioi et al. 2000).”
• PI3K/Akt: getting it right matters (2008, background): “For example, expression of constitutively active mutants or dominant-negative mutants specifically in cardiomyocytes of transgenic mice results in enlarged or reduced heart sizes, respectively (Shioi et al., 2000, 2002).”
• Protein kinase cascades in the regulation of cardiac hypertrophy. (2005, background): “However, a central role of the p110α pathway in IGF-1–induced growth and normal and exercise-induced hypertrophy was demonstrated utilizing mice expressing constitutively active or dominant-negative mutants of PI3K specifically in the heart (22).”