Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathways.

By M. Crackower, G. Oudit, I. Kozieradzki, R. Sarao, Hui Sun, Takehiko Sasaki, E. Hirsch, A. Suzuki, T. Shioi, J. Irie-Sasaki and 13 more. Cell, 2002

616 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d7f8f55f1babc2e3a2c62c86a69e3c40da5f6ac1

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In Cardiology and Cardiovascular Medicine

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Citations in the corpus

The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (2004, background): “, 2002), whereas activation of PI3K leads to increases in cell and organ growth (Leevers et al., 1996; Crackower et al., 2002; Shioi et al., 2002).”
Pten regulates neuronal arborization and social interaction in mice. (2006, positive): “Pten deletion in granule neurons, cardiomyocytes, and the cerebellum induced cellular hypertrophy (Crackower et al., 2002; Kwon et al., 2001).”
Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair (2007, background): “Activation of the PI3K cascade was functionally disrupted by transducing the bifunctional phosphatase PTE”
Role for Akt3/Protein Kinase Bγ in Attainment of Normal Brain Size (2005, background): “This difference might be attributable to more attenuation in the total Akt activity produced by the mutant PI3K or to nonspecific actions of the dominant inhibitory form (19, 65).”
Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “Of the Class I PI3Ks, p110α and p110γ are abundantly expressed in the heart. p110β is also expressed in the heart but at a lower level (Crackower et al., 2002).”
Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy (2005, background): “In particular, PI3Kα hyperactivity has been linked to myocyte hypertroph”
Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “Transgenic mouse models in which PI3K (p110γ) was depleted had enhanced basal contractility but increased susceptibility to pressure overload and ischemic myocardial injury (Crackower et al. 2002; Guo et al. 2010; Oudit and Kassiri 2007; Patrucco et al. 2004).”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “Another way to constitutively activate the PI3K pathway is the cardiomyocyte-specific inactivation of the lipid phosphatase PTEN, which also triggers heart hypertrophy and culminates in reduced cardiac contractility [128].”
Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “In contrast to the effects that are associated with p110α signalling, the phenotype of the p110γ -null mice indicate that this form of PI3K contributes to the generation of pathological hypertrophy and cardiac dysfunction during pressure overload, but is dispensable for postnatal physiological grow”
Protein kinase cascades in the regulation of cardiac hypertrophy. (2005, background): “(23), p110γ is required for stress-induced hypertrophy, but not for normal growth (25, 35).”
Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “PTEN null in heart & muscle (MCK-Cre) Viable Cardiac hypertrophy but normal skeletal muscle growth; unaffected overload-induced muscle hypertrophy; improved muscle regeneration [70,71, 123 ]”
The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism (2006, background): “Accordingly, tissue-specific deletion of PTEN leads to increased cell siz”