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Liver\n                        fibrosis is a significant pathological feature of advanced AE, characterized\n                        by the excessive production and accumulation of extracellular matrix (ECM).\n                        However, the precise underlying mechanism remains largely unknown. In this\n                        study, we show that the long noncoding RNA gm40262, predominantly expressed\n                        in hepatic stellate cells (HSCs), is upregulated in AE. Interestingly, its\n                        knockdown leads to liver fibrosis resolution, accompanied by a substantial\n                        suppression of parasite growth. Gm40262 functions by targeting miR-193b-5p\n                        to activate HSCs and stimulate their proliferation in a\n                        TGF-\u03b2-dependent manner, thereby promoting ECM production by\n                        upregulating Col1\u03b11. Moreover, gm40262 is also involved in\n                        inflammation through the gm40262-miR-193b-5p-TLR4 axis. Our findings suggest\n                        that gm40262 plays a pivotal role in parasite-induced liver fibrosis through\n                        multiple mechanisms, highlighting its potential as a therapeutic target for\n                        hepatic fibrosis.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              <jats:italic toggle=\"yes\">Echinococcus multilocularis<\/jats:italic>\n              is a tiny parasite with\n                        significant medical implications. The chronic parasitism of\n              <jats:italic toggle=\"yes\">E.\n                            multilocularis<\/jats:italic>\n              in the liver generally leads to liver fibrosis,\n                        but the underlying mechanisms are poorly understood. We herein show that\n                        gm40262, a long noncoding RNA predominantly expressed in hepatic stellate\n                        cells (HSCs), is involved in hepatic fibrogenesis during infection by\n                        activating HSCs and promoting extracellular matrix production. The\n                        gm40262-orchestrating fibrogenesis occurs through the\n                        gm40262-miR-193b-5p-TLR4 and gm40262-miR-193b-5p-Col1\u03b11 axes. The\n                        knockdown of gm40262 remarkably alleviates liver fibrosis, with decreased\n                        parasite growth. Our findings reveal a key role of gm40262 in liver fibrosis\n                        during\n              <jats:italic toggle=\"yes\">E. multilocularis<\/jats:italic>\n              infection, rendering it a\n                        therapeutic target for hepatic fibrosis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.02287-24","type":"journal-article","created":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T14:59:16Z","timestamp":1755010756000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["LncRNA gm40262 promotes liver fibrosis and parasite growth through                    the gm40262-miR-193b-5p-TLR4\/Col1\u03b11 axis"],"prefix":"10.1128","volume":"16","author":[{"given":"Tingli","family":"Liu","sequence":"first","affiliation":[{"name":"State Key Laboratory for Animal Disease Control and Prevention, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou 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