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.
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Journal ArticleDOI
Age-Associated Proinflammatory Secretory Phenotype in Vascular Smooth Muscle Cells From the Non-human Primate Macaca mulatta: Reversal by Resveratrol Treatment
Anna Csiszar,Danuta Sosnowska,Mingyi Wang,Edward G. Lakatta,William E. Sonntag,Zoltan Ungvari +5 more
TL;DR: In non-human primates, cell-autonomous activation of nuclear factor κ-light-chain-enhancer of activated B cells and expression of an inflammatory secretome likely contribute to vascular inflammation in aging, and resveratrol treatment prevents the proinflammatory properties of the aged VSMC secretome.
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Longitudinal Perspective on the Conundrum of Central Arterial Stiffness, Blood Pressure, and Aging
Angelo Scuteri,Christopher H. Morrell,Marco Orrù,James B. Strait,Kirill V. Tarasov,Liana Anna Pina Ferreli,Francesco Loi,Maria Grazia Pilia,Alessandro P Delitala,Harold A. Spurgeon,Samer S. Najjar,Majd AlGhatrif,Edward G. Lakatta +12 more
TL;DR: It is indicated that PWV is not a surrogate for BP and that arterial properties other than arterial wall stiffness that vary by age and sex also modulate the BP trajectories during aging and lead to the dissociation of PWV, PP, and SBP trajectories in men.
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The Emergence of a General Theory of the Initiation and Strength of the Heartbeat
TL;DR: The idea that spontaneous SR Ca(2+) releases initiate and regulate normal automaticity provides the key that reunites pacemaker and ventricular cell research, thus evolving a general theory of the initiation and strength of the heartbeat.
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Matrix Metalloproteinases Promote Arterial Remodeling in Aging, Hypertension, and Atherosclerosis
TL;DR: Impressively, MMP inhibition effectively retards/alleviates arterial structural remodeling, decreases stiffness, and improves vascular endothelial function in animal models,3–8 providing a rationale for the translation of MMP actions to therapeutic approaches in aging humans to curb the epidemic of cardiovascular disease.
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Involvement of NADPH oxidase in age-associated cardiac remodeling
TL;DR: Increased RAAS activation may drive age-related cardiac remodeling through the activation of Nox2 NADPH oxidase and subsequent increases in MMP activation, fibrosis and cardiomyocyte hypertrophy.