Over-nutrition contributes to tubulointerstitial fibrosis by targeting nutrient-sensing kinases

Nistala, Ravi; Sowers, James R.; Whaley‐Connell, Adam

doi:10.4161/cc.11.5.19588

Cited by 2 publications

(2 citation statements)

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“…Data support activation of mTOR pathway to early changes in the glomerulus such as mesangial expansion, basement membrane thickening and collagen deposition in the capillary tuft concurrent with mechanisms of proteinuria described above in insulin resistant models (Nistala 2012; Godel 2011; Inoki 2011). Plausible mechanisms may include IKK-β/NF-κB mediated activation of mTOR by cytokines such as TNF-α (Inoki 2011).…”

Section: Insulin Resistance and The Mtor Pathway In Proteinuriasupporting

confidence: 53%

“…Recently, the nutrient sensor serine kinase mTOR has been suggested as the link between over-nutrition, insulin resistance, cardiovascular and kidney injury (Pulakat 2011; Whaley-Connell 2011; Nistala 2012) (Figure 1). Data support activation of mTOR pathway to early changes in the glomerulus such as mesangial expansion, basement membrane thickening and collagen deposition in the capillary tuft concurrent with mechanisms of proteinuria described above in insulin resistant models (Nistala 2012; Godel 2011; Inoki 2011).…”

Section: Insulin Resistance and The Mtor Pathway In Proteinuriamentioning

confidence: 99%

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Resistance to insulin and kidney disease in the cardiorenal metabolic syndrome; role for angiotensin II

Nistala

Whaley‐Connell

2013

Molecular and Cellular Endocrinology

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The presence of insulin resistance is increasingly recognized as an important contributor to early stage kidney disease independent of the contribution of diabetes. Important in this relationship is the strong correlation between hyperinsulinemia and low levels of albuminuria (e.g microalbuminuria). Recent work highlight mechanisms for glomerular/tubulointerstitial injury with excess insulin and emerging evidence identifies a unique role for insulin metabolic signaling and altered handling of salt reabsorption at the level of the proximal tubule. Evidence is also emerging for the role of insulin signaling in the glomerulus both epithelial and endothelial. Central to the mechanism of injury is inappropriate activation of the RAAS.

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