Sodium-Hydrogen Exchanger 3

A sodium-hydrogen antiporter expressed primarily by EPITHELIAL CELLS in the kidneys, it localizes to the apical membrane of the PROXIMAL KIDNEY TUBULE, where it functions in sodium and water reabsorption and possibly calcium homeostasis. It also is expressed in heart, brain, and lung tissues and is resistant to AMILORIDE inhibition.

Also Known As:

Networked: 45 relevant articles (0 outcomes, 4 trials/studies)

Bio-Agent Context: Research Results

Experts

1.	Seidler, Ursula: 3 articles (01/2022 - 10/2002)
2.	Georgescu, Maria-Magdalena: 3 articles (01/2016 - 12/2010)
3.	Li, Xiao C: 3 articles (01/2016 - 10/2015)
4.	Zhuo, Jia L: 3 articles (01/2016 - 10/2015)
5.	Riederer, Brigitte: 2 articles (01/2022 - 01/2012)
6.	Singh, Anurag Kumar: 2 articles (01/2022 - 01/2012)
7.	Koci, Matthew D: 2 articles (11/2016 - 06/2010)
8.	McDonough, Alicia A: 2 articles (01/2016 - 04/2009)
9.	Dudeja, Pradeep K: 2 articles (12/2015 - 11/2008)
10.	Gill, Ravinder K: 2 articles (12/2015 - 11/2008)

Related Diseases

1.	Hypertension (High Blood Pressure) 10/01/2015 - "The present study tested the hypothesis that the Na(+)/H(+) exchanger 3 (NHE3) is required for ANG II-induced hypertension in mice. " 01/01/2016 - "Together, increased local ANG II formation and augmented uptake of circulating ANG II in the proximal tubules, via activation of AT1 (AT1a) receptors and Na(+)/H(+) exchanger 3, may provide a powerful feedforward mechanism for promoting Na(+) retention and the development of ANG II-induced hypertension." 04/01/2009 - "Hypertension provokes differential trafficking of the renal proximal tubule Na(+)/H(+) exchanger 3 (NHE3) to the base of the apical microvilli and Na(+)-P(i) cotransporter 2 (NaPi2) to endosomes. " 07/01/2002 - "NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (pre-hypertensive 1.8-fold; early onset hypertension twofold; established hypertension 1.5-fold; each P < 0.05). " 07/01/2000 - "We conclude that red cell SLC may be a marker of increased NHE-3 protein expression in the proximal tubule, which may account for the blunted pressure natriuresis and predisposition to hypertension."
2.	Inflammation (Inflammations) 01/01/2022 - "A thicker mucus layer, longer crypts and an expanded brush border membrane zone of sodium/hydrogen exchanger 3 (NHE3) abundance may explain the lack of inflammation and the normal fluid absorptive rate in nhe2-/- colon. " 11/01/2016 - "Similarly to that induced by infectious virus, TAstV-2 capsid-induced diarrhea was independent of inflammation or histological changes but was associated with increased intestinal barrier permeability, as well as redistribution of sodium hydrogen exchanger 3 (NHE3) from the membrane to the cytoplasm of the intestinal epithelium. " 10/01/2023 - "A Novel Peptide Prevents Enterotoxin- and Inflammation-Induced Intestinal Fluid Secretion by Stimulating Sodium-Hydrogen Exchanger 3 Activity." 01/01/2022 - "Some preclinical evidence suggests that sodium-glucose cotransporter type 2 inhibitors exert their renoprotective effects by multiple mechanisms, including attenuation of oxidative and endoplasmic reticulum stresses, anti-fibrosis and anti-inflammation, protection of podocytes, suppression of megalin function, improvement of renal hypoxia, restored mitochondrial dysfunction and autophagy, as well as inhibition of sodium-hydrogen exchanger 3. In the present study, the detailed molecular mechanisms of sodium-glucose cotransporter type 2 inhibitors with the actions of diabetic nephropathy were reviewed, with the purpose of providing the basis for drug selection for the treatment of diabetic nephropathy." 12/01/2017 - "There are several mechanisms linking RV-gut interactions via visceral venous congestion which could result in (1) hypoxia and acidosis in enterocytes, which may lead to enhanced sodium-hydrogen exchanger 3 (NHE3) expression with increased sodium and fluid retention; (2) decreased luminal pH in the intestines, which could lead to alteration of the gut microbiome which could increase gut permeability and inflammation; (3) alteration of renal hemodynamics with triggering of the cardiorenal syndrome; and (4) altered phosphate metabolism resulting in increased pulmonary artery stiffening, thereby increasing RV afterload. "
3.	Proteinuria 12/01/2003 - "We have shown previously that proteinuria stimulates the proximal tubular Na(+)/H(+) exchanger 3 (NHE3) in rats. " 10/01/2008 - "These alterations were caused by specific downregulation of the sodium-phosphorus cotransporter, sodium/hydrogen exchanger 3 and aquaporin 2. A Fanconi's-like syndrome was ruled out as there was no proteinuria or glycosuria. " 05/01/2015 - "Tenapanor, a minimally systemically available inhibitor of the intestinal sodium-hydrogen exchanger 3, is being evaluated in clinical trials for its potential to (1) lower gastrointestinal sodium absorption, (2) improve fluid overload-related symptoms, such as hypertension and proteinuria, in patients with CKD, and (3) reduce interdialytic weight gain and intradialytic hypotension in ESRD. "
4.	Hypoxia (Hypoxemia) 01/01/2022 - "Some preclinical evidence suggests that sodium-glucose cotransporter type 2 inhibitors exert their renoprotective effects by multiple mechanisms, including attenuation of oxidative and endoplasmic reticulum stresses, anti-fibrosis and anti-inflammation, protection of podocytes, suppression of megalin function, improvement of renal hypoxia, restored mitochondrial dysfunction and autophagy, as well as inhibition of sodium-hydrogen exchanger 3. In the present study, the detailed molecular mechanisms of sodium-glucose cotransporter type 2 inhibitors with the actions of diabetic nephropathy were reviewed, with the purpose of providing the basis for drug selection for the treatment of diabetic nephropathy." 12/01/2017 - "There are several mechanisms linking RV-gut interactions via visceral venous congestion which could result in (1) hypoxia and acidosis in enterocytes, which may lead to enhanced sodium-hydrogen exchanger 3 (NHE3) expression with increased sodium and fluid retention; (2) decreased luminal pH in the intestines, which could lead to alteration of the gut microbiome which could increase gut permeability and inflammation; (3) alteration of renal hemodynamics with triggering of the cardiorenal syndrome; and (4) altered phosphate metabolism resulting in increased pulmonary artery stiffening, thereby increasing RV afterload. "
5.	Mitochondrial Diseases (Mitochondrial Disease) 01/01/2022 - "Some preclinical evidence suggests that sodium-glucose cotransporter type 2 inhibitors exert their renoprotective effects by multiple mechanisms, including attenuation of oxidative and endoplasmic reticulum stresses, anti-fibrosis and anti-inflammation, protection of podocytes, suppression of megalin function, improvement of renal hypoxia, restored mitochondrial dysfunction and autophagy, as well as inhibition of sodium-hydrogen exchanger 3. In the present study, the detailed molecular mechanisms of sodium-glucose cotransporter type 2 inhibitors with the actions of diabetic nephropathy were reviewed, with the purpose of providing the basis for drug selection for the treatment of diabetic nephropathy."

Related Drugs and Biologics

1.	Sodium
2.	tenapanor
3.	Sodium-Glucose Transport Proteins
4.	Low Density Lipoprotein Receptor-Related Protein-2
5.	Albumins
6.	Messenger RNA (mRNA)
7.	Phosphorus (Red Phosphorus)
8.	Fructose
9.	Catenins
10.	Chloride-Bicarbonate Antiporters

Related Therapies and Procedures

1.	Renal Dialysis (Hemodialysis)