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Jihwan Park

Researcher at University of Pennsylvania

Publications -  53
Citations -  3736

Jihwan Park is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Kidney disease & Kidney. The author has an hindex of 23, co-authored 45 publications receiving 2125 citations. Previous affiliations of Jihwan Park include Gwangju Institute of Science and Technology & Pohang University of Science and Technology.

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Jagged1/Notch2 Controls Kidney Fibrosis via Tfam-mediated Metabolic Reprogramming

TL;DR: JAG1 and NOTCH2 showed the strongest correlation with the degree of interstitial fibrosis in a genome wide expression analysis of a large cohort of human kidney samples and played a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.
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Loss of IL-27Rα Results in Enhanced Tubulointerstitial Fibrosis Associated with Elevated Th17 Responses.

TL;DR: Ex vivo data suggest that endogenous IL-27 acts at several points in the inflammatory cascade to limit the magnitude of immune-mediated damage to the kidney.
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Dnmt3a and Dnmt3b-Decommissioned Fetal Enhancers are Linked to Kidney Disease.

TL;DR: Whole-genome bisulfite sequencing indicated that DnMT3a and Dnmt3b play an important role in methylation of gene regulatory regions that act as fetal-specific enhancers in the developing kidney but are decommissioned in the mature kidney.
Posted ContentDOI

Genome-wide association study of diabetic kidney disease highlights biology involved in renal basement membrane collagen

Rany M. Salem, +105 more
- 19 Dec 2018 - 
TL;DR: The 16 DKD-associated loci provide novel insights into the pathogenesis of DKD, identifying potential biological targets for prevention and treatment.
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The effect of CD4 receptor downregulation and its downstream signaling molecules on HIV-1 latency

TL;DR: It is demonstrated that the HIV-1 latent state is sustained by the reduction of downstream signaling molecules via the downregulation of CD4 and the attenuated activity of transcription factor as AP-1.