ArticlePloS one2013
Na+/H+ exchangers induce autophagy in neurons and inhibit polyglutamine-induced aggregate formation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The potential anti-arrhythmic effect of SGLT2 inhibitors.Cardiovascular diabetology · 2024Review
- Insulin may increase disease severity and mortality of COVID-19 through NaJournal of endocrinological investigation · 2023Article
- Effects of Inhibitors of SLC9A-Type Sodium-Proton Exchangers onMolecular pharmacology · 2022Article
- SLC9A4 in the organum vasculosum of the lamina terminalis is a [NaPflugers Archiv : European journal of physiology · 2020Article
- 22-oxacalcitriol prevents acute kidney injury via inhibition of apoptosis and enhancement of autophagy.Clinical and experimental nephrology · 2019Article
- Intracellular pH Modulates Autophagy and Mitophagy.The Journal of biological chemistry · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In polyglutamine diseases, an abnormally elongated polyglutamine results in protein misfolding and accumulation of intracellular aggregates. Autophagy is a major cellular degradative pathway responsible for eliminating unnecessary proteins, including polyglutamine aggregates. Basal autophagy constitutively occurs at low levels in cells for the performance of homeostatic function, but the regulatory mechanism for basal autophagy remains elusive. Here we show that the Na(+)/H(+) exchanger (NHE) family of ion transporters affect autophagy in a neuron-like cell line (Neuro-2a cells). We showed that expression of NHE1 and NHE5 is correlated to polyglutamine accumulation levels in a cellular model of Huntington's disease, a fatal neurodegenerative disorder characterized by accumulation of polyglutamine-containing aggregate formation in the brain. Furthermore, we showed that loss of NHE5 results in increased polyglutamine accumulation in an animal model of Huntington's disease. Our data suggest that cellular pH regulation by NHE1 and NHE5 plays a role in regulating basal autophagy and thereby promotes autophagy-mediated degradation of proteins including polyglutamine aggregates.
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Registered trials
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