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Swayam Prakash Srivastava

Researcher at Yale University

Publications -  54
Citations -  2343

Swayam Prakash Srivastava is an academic researcher from Yale University. The author has contributed to research in topics: Fibrosis & Diabetes mellitus. The author has an hindex of 25, co-authored 52 publications receiving 1712 citations. Previous affiliations of Swayam Prakash Srivastava include Central Drug Research Institute & Kanazawa Medical University.

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Linagliptin-mediated DPP-4 inhibition ameliorates kidney fibrosis in streptozotocin-induced diabetic mice by inhibiting endothelial-to-mesenchymal transition in a therapeutic regimen

TL;DR: It is found that the DPP-4 inhibitor linagliptin ameliorated kidney fibrosis in diabetic mice without altering the blood glucose levels associated with the inhibition of EndMT and the restoration of microRNA 29s.
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Interactions of DPP-4 and integrin β1 influences endothelial-to-mesenchymal transition

TL;DR: In this article, the DPP-4 inhibitor linagliptin was shown to improve kidney fibrosis and reduce plasma cystatin C levels in diabetic nephropathy mice.
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Healing potential of Calotropis procera on dermal wounds in Guinea pigs.

TL;DR: The present study provides a scientific rationale for the traditional use of this plant in the management of wound healing by markedly increasing collagen, DNA and protein synthesis and epithelisation leading to reduction in wound area.
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MicroRNAs in Kidney Fibrosis and Diabetic Nephropathy: Roles on EMT and EndMT

TL;DR: This review highlights recent advances on the role of miRNAs in the kidney diseases; diabetic nephropathy especially focused on EMT and EndMT program responsible for the development of kidney fibrosis.
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miR-29a levels are elevated in the db/db mice liver and its overexpression leads to attenuation of insulin action on PEPCK gene expression in HepG2 cells.

TL;DR: The results, for the first time, show the effect of miR-29a in counteracting insulin action on PEPCK gene expression by primarily targeting PI3K and abrogating downstream insulin signaling in HepG2 cells.