{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T20:22:23Z","timestamp":1792700543657,"version":"4.5.0"},"reference-count":39,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2017,7,1]],"date-time":"2017-07-01T00:00:00Z","timestamp":1498867200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>\n                      The present study examined the role of\n                      <jats:italic toggle=\"yes\">cystathionine \u03b3-lyase<\/jats:italic>\n                      (CSE) in carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      )-induced liver damage.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      A CSE gene knock-out and luciferase gene knock-in (KI) mouse model was constructed to study the function of CSE and to trace its expression in living status. CCl\n                      <jats:sub>4<\/jats:sub>\n                      or lipopolysaccharide markedly downregulated CSE expression in the liver of mice. CSE-deficient mice showed increased serum alanine aminotransferase and aspartate aminotransferase levels, and liver damage after CCl\n                      <jats:sub>4<\/jats:sub>\n                      challenge, whereas albumin and endogenous hydrogen sulfide (H\n                      <jats:sub>2<\/jats:sub>\n                      S) levels decreased significantly. CSE knockout mice showed increased serum homocysteine levels, upregulation of inflammatory cytokines, and increased autophagy and I\u03baB-\u03b1 degradation in the liver in response to CCl\n                      <jats:sub>4<\/jats:sub>\n                      treatment. The increase in pro-inflammatory cytokines, including tumor necrosis factor-alpha in CSE-deficient mice after CCl\n                      <jats:sub>4<\/jats:sub>\n                      challenge, was accompanied by a significant increase in liver tissue hydroxyproline and \u03b1-smooth muscle actin and histopathologic changes in the liver. However, H\n                      <jats:sub>2<\/jats:sub>\n                      S donor pretreatment effectively attenuated most of these imbalances.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation:<\/jats:title>\n                    <jats:p>\n                      Here, a CSE knock-out and luciferase KI mouse model was established for the first time to study the transcriptional regulation of CSE expression in real time in a non-invasive manner, providing information on the effects and potential mechanisms of CSE on CCl\n                      <jats:sub>4<\/jats:sub>\n                      -induced liver injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      CSE deficiency increases pro-inflammatory cytokines in the liver and exacerbates acute hepatitis and liver fibrosis by reducing H\n                      <jats:sub>2<\/jats:sub>\n                      S production from L-cysteine in the liver. The present data suggest the potential of an H\n                      <jats:sub>2<\/jats:sub>\n                      S donor for the treatment of liver diseases such as toxic hepatitis and fibrosis.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal<\/jats:italic>\n                      . 27, 133\u2013149.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2016.6773","type":"journal-article","created":{"date-parts":[[2016,11,16]],"date-time":"2016-11-16T07:56:22Z","timestamp":1479282982000},"page":"133-149","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":33,"title":["<i>Cystathionine \u03b3-Lyase<\/i>\n                    Deficiency Exacerbates CCl\n                    <sub>4<\/sub>\n                    -Induced Acute Hepatitis and Fibrosis in the Mouse Liver"],"prefix":"10.1177","volume":"27","author":[{"given":"Lei","family":"Ci","sequence":"first","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingyu","family":"Yang","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaowen","family":"Gu","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Li","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]},{"name":"Shanghai Research Center for Model Organisms","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Guo","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziping","family":"Zhou","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengjie","family":"Zhang","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiahao","family":"Shi","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Yang","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhugang","family":"Wang","sequence":"additional","affiliation":[{"name":"Shanghai Research Center for Model Organisms","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Fei","sequence":"additional","affiliation":[{"name":"Tongji University","place":["China"]},{"name":"Shanghai Research Center for Model Organisms","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,7,20]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0144509"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24282"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1590\/S1677-5538.IBJU.2014.0090"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0705891104"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2015.3873"},{"key":"e_1_3_3_7_2","first-page":"644","article-title":"Decreased expression of p38 MAPK mediates protective effects of hydrogen sulfide on hepatic fibrosis","volume":"17","author":"Fan HN","year":"2013","unstructured":"Fan HN, , Wang HJ, , Ren L, , Ren B, , Dan CR, , Li YF, , Hou LZ, , and Deng Y. 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