{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T17:54:55Z","timestamp":1774461295148,"version":"3.50.1"},"reference-count":15,"publisher":"Walter de Gruyter GmbH","issue":"4","license":[{"start":{"date-parts":[[2022,8,1]],"date-time":"2022-08-01T00:00:00Z","timestamp":1659312000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,8,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Kupffer cells (KCs) are the resident macrophages of the liver with similar origins to myeloid-derived macrophages. Once differentiated, KCs exhibit distinct cellular machinery capable of longevity and self-renewal, making them a crucial player in promoting effective intrahepatic communication. However, this gets compromised in disease states like Nonalcoholic Steatohepatitis (NASH), where the loss of embryo-derived KCs (EmKCs) is observed. Despite this, other KC-like and KC-derived populations start to form and contribute to a variety of roles in NASH pathogenesis, often adopting a NASH-associated molecular signature. Here we offer a brief overview of recent reports describing KC polarization and reprogramming in the liver. We describe the complexities of KC cellular identity, their proposed ability to reprogram to fibroblast-like and endothelial-like cells, and the potential implications in NASH.<\/jats:p>","DOI":"10.1515\/mr-2022-0023","type":"journal-article","created":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T03:11:22Z","timestamp":1663643482000},"page":"324-327","source":"Crossref","is-referenced-by-count":5,"title":["The polarizable and reprogrammable identity of Kupffer cells in Nonalcoholic Steatohepatitis"],"prefix":"10.1515","volume":"2","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2754-6092","authenticated-orcid":false,"given":"Tarik","family":"Zahr","sequence":"first","affiliation":[{"name":"Naomi Berrie Diabetes Center , Columbia University , New York , NY , USA"},{"name":"Department of Molecular Pharmacology and Therapeutics , Columbia University , New York , NY , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cell Biology , Columbia University , New York , NY , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Li","family":"Qiang","sequence":"additional","affiliation":[{"name":"Naomi Berrie Diabetes Center , Columbia University , New York , NY , USA"},{"name":"Department of Pathology and Cell Biology , Columbia University , New York , NY , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2022,9,20]]},"reference":[{"key":"2022101709063020127_j_mr-2022-0023_ref_001","doi-asserted-by":"crossref","unstructured":"Sakai, M, Troutman, TD, Seidman, JS, Ouyang, Z, Spann, NJ, Abe, Y, et al.. Liver-derived signals sequentially reprogram myeloid enhancers to initiate and maintain Kupffer cell identity. Immunity 2019;51:655\u201370.e8. https:\/\/doi.org\/10.1016\/j.immuni.2019.09.002.","DOI":"10.1016\/j.immuni.2019.09.002"},{"key":"2022101709063020127_j_mr-2022-0023_ref_002","doi-asserted-by":"crossref","unstructured":"Remmerie, A, Martens, L, Thon\u00e9, T, Castoldi, A, Seurinck, R, Pavie, B, et al.. Osteopontin expression identifies a subset of recruited macrophages distinct from Kupffer cells in the fatty liver. Immunity 2020;53:641\u201357.e14. https:\/\/doi.org\/10.1016\/j.immuni.2020.08.004.","DOI":"10.1016\/j.immuni.2020.08.004"},{"key":"2022101709063020127_j_mr-2022-0023_ref_003","doi-asserted-by":"crossref","unstructured":"Beattie, L, Sawtell, A, Mann, J, Frame, TCM, Teal, B, de Labastida Rivera, F, et al.. Bone marrow-derived and resident liver macrophages display unique transcriptomic signatures but similar biological functions. 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