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Nevertheless, this sequence of events is still far from full understanding with new players and mediators being constantly identified. Originally, the <jats:italic>Hp<\/jats:italic> virulence factors affecting mainly gastric epithelium were proposed to contribute considerably to gastric inflammation, ulceration, and cancer. Furthermore, it has been shown that <jats:italic>Hp<\/jats:italic> possesses the ability to penetrate the mucus layer and directly interact with stroma components including fibroblasts and myofibroblasts. These cells, which are the source of biophysical and biochemical signals providing the proper balance between cell proliferation and differentiation within gastric epithelial stem cell compartment, when exposed to <jats:italic>Hp<\/jats:italic>, can convert into cancer-associated fibroblast (CAF) phenotype. The crosstalk between fibroblasts and myofibroblasts with gastric epithelial cells including stem\/progenitor cell niche involves several pathways mediated by non-coding RNAs, Wnt, BMP, TGF-\u03b2, and Notch signaling ligands. The current review concentrates on the consequences of <jats:italic>Hp<\/jats:italic>-induced increase in gastric fibroblast and myofibroblast number, and their activation towards CAFs with the emphasis to the altered communication between mesenchymal and epithelial cell compartment, which may lead to inflammation, epithelial stem cell overproliferation, disturbed differentiation, and gradual gastric cancer development. Thus, <jats:italic>Hp<\/jats:italic>-activated fibroblasts may constitute the target for anti-cancer treatment and, importantly, for the pharmacotherapies diminishing their activation particularly at the early stages of <jats:italic>Hp<\/jats:italic> infection.<\/jats:p>","DOI":"10.1007\/s10555-023-10122-1","type":"journal-article","created":{"date-parts":[[2023,7,17]],"date-time":"2023-07-17T20:27:24Z","timestamp":1689625644000},"page":"1219-1256","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Helicobacter pylori\u2013activated fibroblasts as a silent partner in gastric cancer development"],"prefix":"10.1007","volume":"42","author":[{"given":"Gracjana","family":"Krzysiek-Maczka","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5805-0065","authenticated-orcid":false,"given":"Tomasz","family":"Brzozowski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agata","family":"Ptak-Belowska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,7,17]]},"reference":[{"key":"10122_CR1","doi-asserted-by":"publisher","unstructured":"Robinson, K., Argent, R. 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