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Jianzhong Wang

Researcher at Chinese PLA General Hospital

Publications -  25
Citations -  808

Jianzhong Wang is an academic researcher from Chinese PLA General Hospital. The author has contributed to research in topics: Angiotensin II & Senescence. The author has an hindex of 16, co-authored 25 publications receiving 733 citations. Previous affiliations of Jianzhong Wang include Chinese General Hospital College of Nursing and Liberal Arts.

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MiR-34 modulates Caenorhabditis elegans lifespan via repressing the autophagy gene atg9

TL;DR: It is reported that a mir-34 loss-of-function mutation in Caenorhabditis elegans markedly delays the age-related physiological decline, extends lifespan, and increases resistance to heat and oxidative stress, and that miR-34 represses autophagy by directly inhibiting the expression of the autophagic-related proteins Atg9 in mammalian cells.
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Downregulation of Connexin 43 Expression by High Glucose Induces Senescence in Glomerular Mesangial Cells

TL;DR: It is demonstrated for the first time that downregulation of Cx43 expression by high glucose promotes the senescence of GMC, which may be involved in the pathogenesis of diabetic nephropathy.
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SIRT3 overexpression antagonizes high glucose accelerated cellular senescence in human diploid fibroblasts via the SIRT3–FOXO1 signaling pathway

TL;DR: It is demonstrated for the first time that Sirtuin 3 overexpression antagonizes high glucose-induced cellular senescence in human diploid fibroblasts via the SIRT3–FOXO1 signaling pathway.
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Mitochondrial Pathway Is Responsible for Aging-Related Increase of Tubular Cell Apoptosis in Renal Ischemia/Reperfusion Injury

TL;DR: It is demonstrated that there was an aging-related increase of tubular cell apoptosis in the renal I/R model, which may be, at least partly, due to an enhanced mitochondrial pathway resulting possibly from increased oxidative stress.
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TIMP-1 Promotes Age-Related Renal Fibrosis Through Upregulating ICAM-1 in Human TIMP-1 Transgenic Mice

TL;DR: The results indicated that TIMP-1 could promote age-related renal fibrosis, which was partly attributed to enhancing inflammation through upregulation of ICAM-1.