{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T05:00:43Z","timestamp":1775624443763,"version":"3.50.1"},"reference-count":226,"publisher":"MDPI AG","issue":"7","license":[{"start":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T00:00:00Z","timestamp":1775260800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Private donation to Rosaria Ingrassia","award":["none"],"award-info":[{"award-number":["none"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Normal steps in uptake of non-heme iron by the gastrointestinal tract include ferrireduction and import across the apical enterocyte membrane by divalent metal transporter 1 (DMT1), responsible for the uptake of non-transferrin bound iron (NTBI). This metal import by the intestinal epithelium requires an acidic milieu generated by the proton pump H(+)\/K(+) ATPase (ATP4). Gastrointestinal uptake of metal can be affected by altering the acid milieu (e.g., proton pump inhibitors). After metal uptake by enterocytes, ferroxidation and export of the metal by ferroportin (FPN) at the basolateral membrane leads to the export of iron bound to transferrin (Tf). In peripheral tissues, cellular uptake of circulating iron is mediated by receptor-mediated endocytosis of Tf-bound iron, with DMT1 transporting the metal out of the endosomal compartment under acidic conditions generated by the vacuolar H+-ATPase. Acidosis is frequently associated with inflammation. The two derangements have relevant consequences like improved solubilization of iron, increased expression of Dmt1, elevated Fe2+ uptake due to DMT1\u2019s ability to cotransport H+, dissociation of Fe-Tf and hepcidin decreasing Fe export via FPN. These changes result in intracellular iron sequestration that frequently becomes noxious. Pharmacological strategies to inhibit NTBI transport are proposed to protect against iron overload associated with acidosis and inflammation.<\/jats:p>","DOI":"10.3390\/ijms27073279","type":"journal-article","created":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T02:06:21Z","timestamp":1775441181000},"page":"3279","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Acidosis, Iron Dyshomeostasis and Inflammatory Injury"],"prefix":"10.3390","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6559-903X","authenticated-orcid":false,"given":"Rosaria","family":"Ingrassia","sequence":"first","affiliation":[{"name":"Section of Biotechnologies, Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew J.","family":"Ghio","sequence":"additional","affiliation":[{"name":"US EPA, Chapel Hill, NC 27599, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7342-6983","authenticated-orcid":false,"given":"Michael","family":"Garrick","sequence":"additional","affiliation":[{"name":"Emeritus of Biochemistry & Pediatrics, University at Buffalo, Buffalo, NY 14260, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,4,4]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"482","DOI":"10.1038\/41343","article-title":"Cloning and characterization of a mammalian proton-coupled metal-ion transporter","volume":"388","author":"Gunshin","year":"1997","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1038\/ng0897-383","article-title":"Microcytic anaemia mice have a mutation in Nramp2, a candidate iron transporter gene","volume":"16","author":"Fleming","year":"1997","journal-title":"Nat. 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