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Meng Zhao

Researcher at Sichuan University

Publications -  19
Citations -  773

Meng Zhao is an academic researcher from Sichuan University. The author has contributed to research in topics: Oxidative stress & Inflammation. The author has an hindex of 11, co-authored 17 publications receiving 213 citations.

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Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance.

TL;DR: In this article, the authors investigated the specific role of mtROS in initiating mitochondrial DNA (mtDNA) damage and inflammation during IRI-AKI, and they found that mt-ROS can promote renal injury by suppressing TFAM-mediated mtDNA maintenance, resulting in decreased mitochondrial energy metabolism and increased cytokine release.
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Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Mitochondrial Damage and Inflammation by Stabilizing Mitochondrial DNA.

TL;DR: In this article, mesenchymal stem cells derived extracellular vesicles (MSC-EVs) were shown to attenuate mtDNA damage and inflammation after acute kidney injury (AKI) and that this effect was at least partially dependent on the mtDNA pathway.
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Injectable extracellular vesicle-released self-assembling peptide nanofiber hydrogel as an enhanced cell-free therapy for tissue regeneration.

TL;DR: It is highlighted that the EV-released KMP2 hydrogel is a promising cell-free therapy for tissue repair, which subsequently decreased chronic renal fibrosis in I/R mice.
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Macrophage-derived extracellular vesicles: diverse mediators of pathology and therapeutics in multiple diseases

TL;DR: An overview of macrophage and EV biology is introduced, primarily focusing on current findings and future perspectives with respect to the pathological and therapeutic effects of Mφ-EVs in various diseases.
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Phloretin ameliorates hyperuricemia-induced chronic renal dysfunction through inhibiting NLRP3 inflammasome and uric acid reabsorption.

TL;DR: Phloretin could effectively attenuate UA-induced renal injury via co-inhibiting NLRP3 and UA reabsorption, and thus it might be a potential therapy to hyperuricemia-related renal diseases.