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Prasanna Krishnamurthy

Researcher at University of Alabama at Birmingham

Publications -  80
Citations -  3265

Prasanna Krishnamurthy is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Stem cell & Inflammation. The author has an hindex of 27, co-authored 73 publications receiving 2524 citations. Previous affiliations of Prasanna Krishnamurthy include East Tennessee State University James H. Quillen College of Medicine & Loyola University Chicago.

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Embryonic Stem Cell-Derived Exosomes Promote Endogenous Repair Mechanisms and Enhance Cardiac Function Following Myocardial Infarction

TL;DR: It is demonstrated that mouse ESC-derived exosomes (mES Ex) possess ability to augment function in infarcted hearts and provide a novel cell-free system that uses the immense regenerative power of ES cells while avoiding the risks associated with direct ES or ES-derived cell transplantation and risk of teratomas.
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IL-10 Inhibits Inflammation and Attenuates Left Ventricular Remodeling After Myocardial Infarction via Activation of STAT3 and Suppression of HuR

TL;DR: It is demonstrated that IL-10 suppresses inflammatory response and contributes to improved LV function and remodeling by inhibiting fibrosis via suppression of HuR/MMP-9 and by enhancing capillary density through activation of STAT3.
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Interleukin-10 deficiency impairs bone marrow-derived endothelial progenitor cell survival and function in ischemic myocardium

TL;DR: In this paper, the IL-10-treatment was shown to increase the survival and function of EPCs after transplantation in the ischemic myocardium, leading to increased EPC retention and their association with the vascular structures.
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MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1.

TL;DR: This study demonstrates that ELAVL1 expression augmented with a concomitant increase in caspase-1 and IL-1 beta expression in human hearts and human ventricular cardiomyocytes under hyperglycemic condition and highlights the potential therapeutic implications of targeting miR-9/ELAVL 1 in preventing cardiomeocyte cell loss during HF in diabetics.