Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.
By I. Shiojima, Kaori Sato, Y. Izumiya, S. Schiekofer, Masahiro Ito, R. Liao, W. Colucci, K. Walsh. Journal of Clinical Investigation, 2005
955 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/acec0996a57b8f1966097640a10022e9b641c0e0
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
In Molecular Biology
Citations in the corpus
- Tet2-mediated Clonal Hematopoiesis Accelerates Heart Failure through a Mechanism Involving the IL-1β/NLRP3 Inflammasome (2018, background): “The TAC model initially induces a cardiac hypertrophic response to pressure overload, and this is followed by systolic dysfunction in response to capillary rarefaction (33,34).”
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “…supply to hypertrophying myocytes, as disruption of angiogenesis during adaptive hypertrophy leads to contractile dysfunction (Izumiya et al. 2006; Shiojima et al. 2005), while stimulation of angiogenesis during pressure overload is protective and prevents the transition from compensatory cardiac…”
- The protective role of estrogen and estrogen receptors in cardiovascular disease and the controversial use of estrogen therapy (2017, background): “Increased cardiac angiogenesis is necessary to maintain LV function during adaptive hypertrophy and compensated heart hypertrophy as the larger LV has an obvious need for more blood vessels [56, 57].”
- Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “To resolve this potential paradox, a conditional transgenic system was employe”
- Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2 (2013, background): “Furthermore, capillary growth does not keep pace with myocyte growth in disease models, which, in concert with fibrotic change, limits oxygen delivery to the myocardium.(71,72)”