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How\n              <jats:italic>Mtb<\/jats:italic>\n              escapes this immune attack remains elusive. In this study, we unveiled a novel regulatory mechanism by which SIRT7 regulates cytoskeletal remodeling by modulating RAC1 activation. We discovered that SIRT7 expression was significantly reduced in CD14\n              <jats:sup>+<\/jats:sup>\n              monocytes of TB patients.\n              <jats:italic>Mtb<\/jats:italic>\n              infection diminished SIRT7 expression by macrophages at both the mRNA and protein levels. SIRT7 deficiency impaired actin cytoskeleton-dependent macrophage phagocytosis, LC3II expression, and bactericidal activity. In a murine tuberculosis model, SIRT7 deficiency detrimentally impacted host resistance to\n              <jats:italic>Mtb<\/jats:italic>\n              , while\n              <jats:italic>Sirt7<\/jats:italic>\n              overexpression significantly increased the host defense against\n              <jats:italic>Mtb<\/jats:italic>\n              , as determined by bacterial burden and inflammatory\u2013histopathological damage in the lung. Mechanistically, we demonstrated that SIRT7 limits\n              <jats:italic>Mtb<\/jats:italic>\n              infection by directly interacting with and activating RAC1, through which cytoskeletal remodeling is modulated. Therefore, we concluded that SIRT7, in its role regulating cytoskeletal remodeling through RAC1, is critical for host responses during\n              <jats:italic>Mtb<\/jats:italic>\n              infection and proposes a potential target for tuberculosis treatment.\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE<\/jats:title>\n              <jats:p>\n                Tuberculosis (TB), caused by\n                <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                (\n                <jats:italic>Mtb<\/jats:italic>\n                ), remains a significant global health issue. Critical to macrophages\u2019 defense against\n                <jats:italic>Mtb<\/jats:italic>\n                is phagocytosis, governed by the actin cytoskeleton. Previous research has revealed that\n                <jats:italic>Mtb<\/jats:italic>\n                manipulates and disrupts the host\u2019s actin network, though the specific mechanisms have been elusive. Our study identifies a pivotal role for SIRT7 in this context:\n                <jats:italic>Mtb<\/jats:italic>\n                infection leads to reduced SIRT7 expression, which, in turn, diminishes RAC1 activation and consequently impairs actin-dependent phagocytosis. The significance of our research is that SIRT7 directly engages with and activates Rac Family Small GTPase 1 (RAC1), thus promoting effective phagocytosis and the elimination of\n                <jats:italic>Mtb<\/jats:italic>\n                . This insight into the dynamic between host and pathogen in TB not only broadens our understanding but also opens new avenues for therapeutic development.\n              <\/jats:p>\n            <\/jats:sec>\n          <\/jats:sec>","DOI":"10.1128\/mbio.00756-24","type":"journal-article","created":{"date-parts":[[2024,9,17]],"date-time":"2024-09-17T17:01:26Z","timestamp":1726592486000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":8,"title":["SIRT7 remodels the cytoskeleton\n            <i>via<\/i>\n            RAC1 to enhance host resistance to\n            <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.1128","volume":"15","author":[{"given":"Fuxiang","family":"Li","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China"},{"name":"Department of Biochemistry, Center for Molecular Biomedicine (CMB), Friedrich Schiller University Jena, Jena, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ximeng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinjin","family":"Xu","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Pharmaceutical Sciences, Shenzhen University Medical School, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Xiangya Hospital, Central South University, Changsha, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xirui","family":"Yang","sequence":"additional","affiliation":[{"name":"Dornsife College of Letters, Arts and Sciences, University of Southern California, Los Angeles, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guofang","family":"Deng","sequence":"additional","affiliation":[{"name":"Guangdong Key Lab for Diagnosis &amp; Treatment of Emerging Infectious Diseases, Shenzhen Third People\u2019s Hospital, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youchao","family":"Dai","sequence":"additional","affiliation":[{"name":"Guangzhou Eighth People\u2019s Hospital, Guangzhou Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baohua","family":"Liu","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory for Systemic Aging and Intervention (SAI), National Engineering Research Center for Biotechnology (Shenzhen), International Cancer Center, Shenzhen University, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8387-3653","authenticated-orcid":false,"given":"Christian","family":"Kosan","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Center for Molecular Biomedicine (CMB), Friedrich Schiller University Jena, Jena, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2101-9013","authenticated-orcid":true,"given":"Xinchun","family":"Chen","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1363-2328","authenticated-orcid":true,"given":"Yi","family":"Cai","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_4_2_2","volume-title":"Global tuberculosis report 2023","author":"World Health Organization","year":"2023","unstructured":"World Health Organization. 2023. 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