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Feng Zhang

Researcher at Fudan University

Publications -  2715
Citations -  225233

Feng Zhang is an academic researcher from Fudan University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 172, co-authored 1278 publications receiving 181865 citations. Previous affiliations of Feng Zhang include Cincinnati Children's Hospital Medical Center & Nanjing Medical University.

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N-acetylcysteine attenuates reactive-oxygen-species-mediated endoplasmic reticulum stress during liver ischemia-reperfusion injury

TL;DR: This study provides new evidence for the protective effects of NAC treatment on hepatocytes during IRI through inhibition of ROS-mediated ER stress, NAC may be critical to inhibit the ER-stress-related apoptosis pathway.
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Mapping a functional cancer genome atlas of tumor suppressors in mouse liver using AAV-CRISPR–mediated direct in vivo screening

TL;DR: AAV-mediated autochthonous CRISPR screens provide a powerful means for mapping a provisional functional cancer genome atlas of tumor suppressors in vivo, revealing the functional consequence of multiple variants in driving liver tumorigenesis in immunocompetent mice.
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Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis.

TL;DR: Results indicate that salusin-β promotes VSMC proliferation via cAMP-PKA-EGFR-CREB/ERK pathway and vascular fibrosis via TGF-β1-Smad pathway and contributes to vascular remodeling and hypertension.
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Identifying potential risk haplotypes for schizophrenia at the DTNBP1 locus in Han Chinese and Scottish populations

TL;DR: In this paper, the dystrobrevin-binding protein 1 (DTNBP1) gene on chromosome 6p has emerged as a potential susceptibility gene for schizophrenia, and a number of attempts to replicate the original association finding have been successful, they have not identified any obvious pathogenic variants or a single at risk haplotype common to all populations studied.
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Salusin-β contributes to oxidative stress and inflammation in diabetic cardiomyopathy.

TL;DR: It is indicated that salusin-β contributes to inflammation in DCM via NOX2/ROS/NFκB signaling, and that knockdown of salusIn-β attenuates cardiac dysfunction, oxidative stress and inflammation inDCM.