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Autophagy related 5 (Atg5) is a key protein involved in phagocytic membrane elongation in autophagic vesicles that forms a complex with Atg12 and Atg16L1. Alterations in <jats:italic>Atg5<\/jats:italic> are related to both acute and chronic kidney diseases in experimental models. However, the role of macrophage-expressed <jats:italic>Atg5<\/jats:italic> in acute kidney injury remains unclear.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Using a myeloid cell-specific <jats:italic>Atg5<\/jats:italic> knockout (<jats:italic>M\u03a6 atg5<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) mouse, we established renal ischemia\/reperfusion and unilateral ureteral obstruction models to evaluate the role of macrophage <jats:italic>Atg5<\/jats:italic> in renal macrophage migration and fibrosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Based on changes in the serum urea nitrogen and creatinine levels, <jats:italic>Atg5<\/jats:italic> deletion had a minimal effect on renal function in the early stages after mild injury; however, M<jats:italic>\u03a6 atg5<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice had reduced renal fibrosis and reduced macrophage recruitment after 4 weeks of ischemia\/reperfusion injury and 2 weeks of unilateral ureteral obstruction injury. <jats:italic>Atg5<\/jats:italic> deficiency impaired the CCL20-CCR6 axis after severe ischemic kidneys. Chemotactic responses of bone marrow-derived monocytes (BMDMs) from M\u03a6 <jats:italic>atg5<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice to CCL20 were significantly attenuated compared with those of wild-type BMDMs, and this might be caused by the inhibition of PI3K, AKT, and ERK1\/2 activation.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Our data indicate that <jats:italic>Atg5<\/jats:italic> deficiency decreased macrophage migration by impairing the CCL20-CCR6 axis and inhibited M2 polarization, thereby improving kidney fibrosis.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12964-024-01600-2","type":"journal-article","created":{"date-parts":[[2024,4,9]],"date-time":"2024-04-09T11:02:02Z","timestamp":1712660522000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Atg5 deficiency in macrophages protects against kidney fibrosis via the CCR6-CCL20 axis"],"prefix":"10.1186","volume":"22","author":[{"given":"Yufeng","family":"Zhu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiexing","family":"Tan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanzhan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuhong","family":"Gong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyong","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziguo","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinyu","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huifang","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiming","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaotao","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Gong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,4,9]]},"reference":[{"key":"1600_CR1","doi-asserted-by":"publisher","first-page":"293","DOI":"10.1146\/annurev-med-050214-013407","volume":"67","author":"A Zuk","year":"2016","unstructured":"Zuk A, Bonventre JV. 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