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
Stimulation of P2Y receptors activates c-fos gene expression and inhibits DNA synthesis in cultured cardiac fibroblasts
Jing Sheng Zheng,Lydia O'Neill,Xilin Long,Tania E. Webb,Eric A. Barnard,Edward G. Lakatta,Marvin O. Boluyt +6 more
TL;DR: The findings suggest that the effects of ATP on [3H]thymidine incorporation into DNA and on expression of c-fos mRNA are exerted via distinct P2Y receptor subtypes.
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Paracrine effects of hypoxic fibroblast-derived factors on the MPT-ROS threshold and viability of adult rat cardiac myocytes.
K. Shivakumar,Steven J. Sollott,M. Sangeetha,S. Sapna,Bruce D. Ziman,Shaomeng Wang,Edward G. Lakatta +6 more
TL;DR: Because both hypoxia and oxidant stress prevail in a setting of ischemia and reperfusion, the effects of soluble factors from hypoxic fibroblasts on the MPT-ROS threshold and viability of myocytes may represent a novel paracrine mechanism that could exacerbate ischemIA-reperfusion injury to cardiomyocytes.
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RGS2 Is a Primary Terminator of β2-Adrenergic Receptor-Mediated Gi Signaling
Khalid Chakir,Weizhong Zhu,Sharon Tsang,Anthony Yiu-Ho Woo,Anthony Yiu-Ho Woo,Dongmei Yang,Xianhua Wang,Xianhua Wang,Xiaokun Zeng,Man Hee Rhee,Ulrike Mende,Norimichi Koitabashi,Eiki Takimoto,Kendall J. Blumer,Edward G. Lakatta,David A. Kass,Rui-Ping Xiao,Rui-Ping Xiao +17 more
TL;DR: RGS2 is defined as a novel negative regulator of the β(2)AR-G(i) signaling but also provides a potential novel target for the treatment of chronic heart failure.
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Diminished cardiac hypertrophy and muscle performance in older compared with younger adult rats with chronic atrioventricular block
TL;DR: During long-term block, age exerted not only a significant effect on the extent of cardiac hypertrophy but also an independentEffect on the developed tension of cardiac muscle.
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Quantitative proteomic analysis reveals novel mitochondrial targets of estrogen deficiency in the aged female rat heart.
Timothy S. Lancaster,Sarah J. Jefferson,J. Craig Hunter,Veronica Lopez,J. E. Van Eyk,Edward G. Lakatta,Donna H. Korzick +6 more
TL;DR: Age-dependent alterations in mitochondrial signaling indicate a highly selective myocardial response to E(2) deficiency, and the combined proteomic and functional approaches described here offer possibility of new protein targets for experimentation and therapeutic intervention in the aged female population.