scispace - formally typeset
E

Edward G. Lakatta

Researcher at National Institutes of Health

Publications -  902
Citations -  95504

Edward G. Lakatta is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Blood pressure & Population. The author has an hindex of 146, co-authored 858 publications receiving 88637 citations. Previous affiliations of Edward G. Lakatta include University of Pittsburgh & University College London.

Papers
More filters
Journal ArticleDOI

The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals

Georg Ehret, +375 more
- 01 Oct 2016 - 
TL;DR: In this article, the authors identified 66 blood pressure-associated loci, of which 17 were new; 15 harbored multiple distinct association signals, and 66 index SNPs were enriched for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary role in blood pressure control through modulation of vascular tone across multiple tissues.
Journal ArticleDOI

Diminished inotropic response of aged myocardium to catecholamines.

TL;DR: It is concluded that the intrinsic inotropic response to catecholamines is diminished in the aged myocardium and this finding does not appear to result from differences in tachyphylaxis, tissue uptake of catechlamines, or the ability of the contractile proteins to respond to increasing concentrations of calcium but instead may result from a decreased ability of ctcholamines to increase the intracellular calcium available for contraction.
Journal ArticleDOI

Increased cardiomyocyte apoptosis during the transition to heart failure in the spontaneously hypertensive rat.

TL;DR: Increased numbers of apoptotic cells are present in failing SHR hearts, suggesting that apoptosis might be a mechanism involved in the reduction of myocyte mass that accompanies the transition from stable compensation to heart failure in this model.
Journal ArticleDOI

Migration of cultured vascular smooth muscle cells through a basement membrane barrier requires type IV collagenase activity and is inhibited by cellular differentiation.

TL;DR: Results suggest that VSMC migration in vivo may be dependent on MMP2 activity, which could be regulated by the phenotypic state of VSMCs and increase as these cells undergo the transition from a quiescent and differentiated state to that of a dedifferentiated, proliferating, and motile phenotype after injury to the vessel.
Journal ArticleDOI

p53 and the hypoxia-induced apoptosis of cultured neonatal rat cardiac myocytes.

TL;DR: The results suggest that the intracellular signaling pathways activated by p53 might play a critical role in the regulation of hypoxia-induced apoptosis of cardiomyocytes.