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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Deciphering the mechanisms of the Na+/H+ exchanger-3 regulation in organ dysfunction

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Author(s):
Girardi, Adriana C. C. [1] ; Di Sole, Francesca [2, 3]
Total Authors: 2
Affiliation:
[1] Univ Sao Paulo, Sch Med, Heart Inst InCor, Sao Paulo - Brazil
[2] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 - USA
[3] Univ Texas SW Med Ctr Dallas, Ctr Mineral Metab & Clin Res, Dallas, TX 75390 - USA
Total Affiliations: 3
Document type: Review article
Source: AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY; v. 302, n. 11, p. C1569-C1587, JUN 2012.
Web of Science Citations: 44
Abstract

Girardi AC, Di Sole F. Deciphering the mechanisms of the Na+/H+ exchanger-3 regulation in organ dysfunction. Am J Physiol Cell Physiol 302: C1569-C1587, 2012. First published March 28, 2012; doi:10.1152/ajpcell.00017.2012.-The Na+/H+ exchanger-3 (NHE3) belongs to the mammalian NHE protein family and catalyzes the electro-neutral exchange of extracellular sodium for intracellular proton across cellular membranes. Its transport function is of essential importance for the maintenance of the body's salt and water homeostasis as well as acid-base balance. Indeed, NHE3 activity is finely regulated by a variety of stimuli, both acutely and chronically, and its transport function is fundamental for a multiplicity of severe and world-wide infection-pathological conditions. This review aims to provide a concise overview of NHE3 physiology and discusses the role of NHE3 in clinical conditions of prominent importance, specifically in hypertension, diabetic nephropathy, heart failure, acute kidney injury, and diarrhea. Study of NHE3 function in models of these diseases has contributed to the deciphering of mechanisms that control the delicate ion balance disrupted in these disorders. The majority of the findings indicate that NHE3 transport function is activated before the onset of hypertension and inhibited thereafter; NHE3 transport function is also upregulated in diabetic nephropathy and heart failure, while it is reported to be downregulated in acute kidney injury and in diarrhea. The molecular mechanisms activated during these pathological conditions to regulate NHE3 transport function are examined with the aim of linking NHE3 dysfunction to the analyzed clinical disorders. (AU)