{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T01:06:59Z","timestamp":1788052019411,"version":"build-2784847793"},"reference-count":86,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T00:00:00Z","timestamp":1760313600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    (\n                    <jats:italic>H. pylori<\/jats:italic>\n                    ), a key gastric mucosal pathogen, causes chronic gastritis, peptic ulcers, and gastric cancer.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    remodel the gastric microenvironment through metabolic reprogramming to drive pathogenesis. CagA\n                    <jats:sup>+<\/jats:sup>\n                    strains disrupt lipid metabolism, increasing non-alcoholic fatty liver disease, cardiovascular, and Alzheimer\u2019s risks via PPAR interference,\n                    <jats:italic>GBA1<\/jats:italic>\n                    demethylation, and altered FABP1\/APOA1 expression, reversible by eradication. In glucose metabolism,\n                    <jats:italic>H. pylori<\/jats:italic>\n                    promote carcinogenesis via Lonp1-induced glycolysis, PDK1\/Akt dysregulation, and HKDC1\/TGF-\u03b21\/MDFI-mediated epithelial-mesenchymal transition, while exacerbating high-fat diet-induced dysbiosis. Infection manipulates macrophage immunometabolism. Bacterial utilization of host L-lactate through\n                    <jats:italic>H. pylori<\/jats:italic>\n                    gene clusters enables proliferation, gland colonization, and immune evasion by suppressing complement activation and TNF\/IL-6 secretion. Lactate-targeting strategies show therapeutic promise. Amino acid dysregulation involves\n                    <jats:italic>H. pylori<\/jats:italic>\n                    biotin protein ligase (HpBPL)-mediated catabolism and \u03b3-glutamyl transpeptidase-induced glutathione hydrolysis, depleting antioxidants while inducing dendritic cell tolerance. branched-chain amino acids accumulation activates mTORC1, and cystine-glutamate transporter inhibition with miR-30b upregulation exacerbates mucosal damage, forming a self-sustaining \u201cmetabolic reprogramming-immune evasion-tissue destruction\u201d cycle. These mechanisms collectively enable\n                    <jats:italic>H. pylori<\/jats:italic>\n                    to propel gastric carcinogenesis, highlighting metabolism-targeted interventions as future solutions. This review summarizes how\n                    <jats:italic>H. pylori<\/jats:italic>\n                    remodel the gastric microenvironment and drives pathogenesis by manipulating host lipid, glucose, lactate, and amino acid metabolism.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2025.1678044","type":"journal-article","created":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T05:27:31Z","timestamp":1760333251000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Metabolic reprogramming in Helicobacter pylori infection: from mechanisms to therapeutics"],"prefix":"10.3389","volume":"15","author":[{"given":"Tong","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuelin","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Cai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minglin","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,10,13]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/hel.12537","article-title":"Helicobacter pylori and non-alcoholic fatty liver disease: A new enigma","volume":"23","author":"Abdel-Razik","year":"2018","journal-title":"Helicobacter"},{"key":"B2","doi-asserted-by":"publisher","first-page":"823","DOI":"10.1136\/gutjnl-2019-320234","article-title":"Is gastric cancer becoming a rare disease? 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