Adiponectin regulates albuminuria and podocyte function in mice.

By K. Sharma, S. RamachandraRao, G. Qiu, H. Usui, Yanqing Zhu, S. Dunn, R. Ouedraogo, K. Hough, P. McCue, L. Chan and 2 more. Journal of Clinical Investigation, 2008

636 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Oncology

View Paper: https://www.semanticscholar.org/paper/3c3be7831cb64f2c49c5e5b6e2623a5daac105c3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. J. Forbes
2. P. Scherer
3. M. Cooper
4. Haiming Cao
5. M. Blüher

In Epidemiology

1. P. Scherer
2. Sushil Kumar Jain
3. Prasenjit Manna
4. Haiming Cao
5. M. Blüher

Citations in the corpus

• Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “The adipokine leptin enhances the action of insulin on both the inhibition of hepatic glucose production and on glucose uptake,256 which may perhaps explain the role of insulin in relation to insulin sensitivity.257 It has been observed that plasma leptin concentrations are independently associated ”
• Adiponectin: mechanistic insights and clinical implications (2012, background): “Lack of adiponectin has been linked to increased podocyte injury and albuminuria in adiponectin gene knockout (Adipoq) mouse models, with adiponectin therapies potentially reversing some renal dysfunction [33, 34].”
• Molecular mechanisms of diabetic kidney disease. (2014, neutral): “In podocytes AMPK negatively regulates the NADPH oxidase NOX4 and oxidative stress (44, 83).”
• Adiponectin Regulation and Function (2018, neutral): “Adiponectin knockout mice have albuminuria, glomerular hypertrophy, tubulointerstitial fibrosis, and podocyte foot process effacement, which is reversed upon adiponectin administration (65,221,296,398).”
• Mechanisms of diabetic complications. (2013, background): “Indeed, a loss of serine473 Akt phosphorylation has been identified at sites of diabetic complications (538, 637) particularly in models of type 2 diabetes.”