{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T16:16:07Z","timestamp":1790957767224,"version":"4.1.0"},"reference-count":183,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,1,1]]},"abstract":"<jats:p>Non-alcoholic fatty liver disease (NAFLD) with its more progressive form non-alcoholic steatohepatitis (NASH) has become the most common chronic liver disease, thereby representing a great burden for patients and healthcare systems. Specific pharmacological therapies for NAFLD are still missing. Inflammation is an important driver in the pathogenesis of NASH, and the mechanisms underlying inflammation in NAFLD represent possible therapeutic targets. In NASH, various intra- and extrahepatic triggers involved in the metabolic injury typically lead to the activation of different immune cells. This includes hepatic Kupffer cells, i.e. liver-resident macrophages, which can adopt an inflammatory phenotype and activate other immune cells by releasing inflammatory cytokines. As inflammation progresses, Kupffer cells are increasingly replaced by monocyte-derived macrophages with a distinct lipid-associated and scar-associated phenotype. Many other immune cells, including neutrophils, T lymphocytes \u2013 such as auto-aggressive cytotoxic as well as regulatory T cells \u2013 and innate lymphoid cells balance the progression and regression of inflammation and subsequent fibrosis. The detailed understanding of inflammatory cell subsets and their activation pathways prompted preclinical and clinical exploration of potential targets in NAFLD\/NASH. These approaches to target inflammation in NASH include inhibition of immune cell recruitment via chemokine receptors (e.g. cenicriviroc), neutralization of CD44 or galectin-3 as well as agonism to nuclear factors like peroxisome proliferator-activated receptors and farnesoid X receptor that interfere with the activation of immune cells. As some of these approaches did not demonstrate convincing efficacy as monotherapies, a rational and personalized combination of therapeutic interventions may be needed for the near future.<\/jats:p>","DOI":"10.1530\/joe-22-0194","type":"journal-article","created":{"date-parts":[[2022,10,19]],"date-time":"2022-10-19T10:19:36Z","timestamp":1666174776000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":45,"title":["Treating inflammation to combat non-alcoholic fatty liver disease"],"prefix":"10.1530","volume":"256","author":[{"given":"Leke","family":"Wiering","sequence":"first","affiliation":[{"name":"Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt-Universit\u00e4t zu Berlin, Department of Hepatology and Gastroenterology, Campus Virchow-Klinikum and Campus Charit\u00e9 Mitte, Berlin, Germany"},{"name":"Berlin Institute of Health at Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, BIH Biomedical Innovation Academy, BIH Charit\u00e9 Junior Clinician Scientist Program, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6206-0226","authenticated-orcid":true,"given":"Frank","family":"Tacke","sequence":"additional","affiliation":[{"name":"Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt-Universit\u00e4t zu Berlin, Department of Hepatology and Gastroenterology, Campus Virchow-Klinikum and Campus Charit\u00e9 Mitte, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"International Journal of Molecular Sciences","doi-asserted-by":"publisher","first-page":"1649","DOI":"10.3390\/ijms18081649","article-title":"Adipokines and non-alcoholic fatty liver disease: multiple interactions","volume":"18","author":"Adolph","year":"2017","unstructured":"Adolph TEGrander CGrabherr FTilg H2017Adipokines and non-alcoholic fatty liver disease: multiple interactions. 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