Kallistatin protects against diabetic nephropathy in db/db mice by suppressing AGE-RAGE-induced oxidative stress. (Q46644065)

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29 February 2020

title

Kallistatin protects against diabetic nephropathy in db/db mice by suppressing AGE-RAGE-induced oxidative stress (English)

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29 February 2020

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2

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Haojia Wu

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Hui Y Lan

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Sydney C W Tang

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author name string

Wai Han Yiu

1

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Rui Xi Li

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Irene Yam

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Loretta Y Y Chan

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Joseph C K Leung

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Kar Neng Lai

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language of work or name

English

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publication date

1 February 2016

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29 February 2020

volume

89

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page(s)

386-398

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issue

2

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https://scigraph.springernature.com/pub.10.1038/ki.2015.331

29 February 2020

exact match

0 references

cites work

Oxidative stress: meeting multiple targets in pathogenesis of diabetic nephropathy

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Clinical review: The role of advanced glycation end products in progression and complications of diabetes

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Differential effects of advanced glycation end-products on renal tubular cell inflammation

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Dipeptidyl peptidase-4 deficiency protects against experimental diabetic nephropathy partly by blocking the advanced glycation end products-receptor axis.

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Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis

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Targeting the AGE-RAGE axis improves renal function in the context of a healthy diet low in advanced glycation end-product content

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The tubulointerstitium in progressive diabetic kidney disease: more than an aftermath of glomerular injury?

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Diabetic tubulopathy: an emerging entity.

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Activation of tubular epithelial cells in diabetic nephropathy and the role of the peroxisome proliferator-activated receptor-gamma agonist

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Bradykinin and high glucose promote renal tubular inflammation.

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Toll-like receptor 4 promotes tubular inflammation in diabetic nephropathy

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BMP7 reduces inflammation and oxidative stress in diabetic tubulopathy.

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Kallistatin, a novel human tissue kallikrein inhibitor: levels in body fluids, blood cells, and tissues in health and disease

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Immunolocalization and expression of kallistatin and tissue kallikrein in human inflammatory bowel disease.

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Cellular localization of tissue kallikrein and kallistatin mRNAs in human kidney

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Kallistatin attenuates endothelial apoptosis through inhibition of oxidative stress and activation of Akt-eNOS signaling

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7 January 2021

Kallistatin is a new inhibitor of angiogenesis and tumor growth

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Kallistatin inhibits vascular inflammation by antagonizing tumor necrosis factor-alpha-induced nuclear factor kappaB activation

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Inhibition of angiogenesis and HCT-116 xenograft tumor growth in mice by kallistatin

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Protection effect of kallistatin on carbon tetrachloride-induced liver fibrosis in rats via antioxidative stress

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Protection of the liver against CCl4-induced injury by intramuscular electrotransfer of a kallistatin-encoding plasmid

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Human kallistatin administration reduces organ injury and improves survival in a mouse model of polymicrobial sepsis

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Salutary effect of kallistatin in salt-induced renal injury, inflammation, and fibrosis via antioxidative stress

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Tissue kallikrein mediates pro-inflammatory pathways and activation of protease-activated receptor-4 in proximal tubular epithelial cells

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Kallistatin, a novel anti-angiogenesis agent, inhibits angiogenesis via inhibition of the NF-κB signaling pathway.

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Depletion of endogenous kallistatin exacerbates renal and cardiovascular oxidative stress, inflammation, and organ remodeling

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Prophylactic adenovirus-mediated human kallistatin gene therapy suppresses rat arthritis by inhibiting angiogenesis and inflammation

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7 January 2021

Adenovirus-mediated kallistatin gene transfer ameliorates disease progression in a rat model of osteoarthritis induced by anterior cruciate ligament transection

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Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy

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Effects of kallistatin on oxidative stress and inflammation on renal ischemia-reperfusion injury in mice.

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Antiangiogenic and antineuroinflammatory effects of kallistatin through interactions with the canonical Wnt pathway

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Kallistatin antagonizes Wnt/β-catenin signaling and cancer cell motility via binding to low-density lipoprotein receptor-related protein 6

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Elevated circulation levels of an antiangiogenic SERPIN in patients with diabetic microvascular complications impair wound healing through suppression of Wnt signaling

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Additive renoprotective effects of B2-kinin receptor blocker and PPAR-γ agonist in uninephrectomized db/db mice.

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miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes.

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Identifiers

DOI

10.1038/KI.2015.331

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:26536000%20AND%20SRC:MED&resulttype=core&format=json

29 February 2020

1 reference