Cited by 17Ion Transport and Channel RegulationLiver physiology and pathologyDrug Transport and Resistance Mechanisms

Pathophysiology of hepatic Na+/H+ exchange (Review)

Open access
Li, Tingting, Tuo, Biguang·2020·Experimental and Therapeutic Medicine

Abstract

Na+/H+ exchangers (NHEs) are a family of membrane proteins that contribute to exchanging one intracellular proton for one extracellular sodium. The family of NHEs consists of nine known members, NHE1‑9. Each isoform represents a different gene product that has unique tissue expression, membrane localization, physiological effects, pathological regulation and sensitivity to drug inhibitors. NHE1 was the first to be discovered and is often referred to as the ‘housekeeping’ isoform of the NHE family. NHEs are not only involved in a variety of physiological processes, including the control of transepithelial Na+ absorption, intracellular pH, cell volume, cell proliferation, migration and apoptosis, but also modulate complex pathological events. Currently, the vast majority of review articles have focused on the role of members of the NHE family in inflammatory bowel disease, intestinal infectious diarrhea and digestive system tumorigenesis, but only a few reviews have discussed the role of NHEs in liver disease. Therefore, the present review described the basic biology of NHEs and highlighted their physiological and pathological effects in the liver.

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Crossref · 10.3892/etm.2020.8888

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  • Intracellular alkalinization mediated by the sodium hydrogen exchanger is a permissive signal for DNA synthesis and mitotic activity.

    “In fact, the intracellular alkalinization mediated by sodium hydrogen exchanger has been identified as a permissive signal for DNA synthesis and mitotic activity[78].”

    From Liver regeneration after partial hepatectomy: Triggers and mechanisms (2025) · cites this paper as [78]

    Section 3, “NHEs in hepatic physiological regulation” (page unavailable), says that NHE activation promotes hepatocyte proliferation and that EGF stimulates NHEs before DNA synthesis increases. It describes NHE1-mediated intracellular alkalinization as a possible antiapoptotic signal, but does not identify that alkalinization as a permissive signal for DNA synthesis or mitotic activity. (LLM, conf=0.83)

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Authors
Li, T., & Tuo, B.
Affiliations
Zunyi Medical University (CN)
Venue
Experimental and Therapeutic Medicine
Published
2020-06-12
Volume
20
Issue
2
Pages
1220-1229
ISSN
  • 1792-0981 (ISSN-L)
  • 1792-1015
OpenAlex
W3035089602
Cited by
17
References
155
Citations by year
2025: 4 · 2024: 1 · 2023: 2 · 2022: 7 · 2021: 2 · 2020: 1
FWCI
0.29
Type
journal article
Language
en
Open access
Locations
  • Experimental and Therapeutic Medicine (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Keywords
Na+/H+ exchanger, NHE1, NHE2, NHE3, NHE6, NHE8, NHE9, liver disease, intracellular pH regulation, cell volume regulation

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