{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T04:29:15Z","timestamp":1780547355148,"version":"3.54.1"},"reference-count":52,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2017,10,1]],"date-time":"2017-10-01T00:00:00Z","timestamp":1506816000000},"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":[[2017,10]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>\n                      Methionine sulfoxide reductase A (MsrA), which is abundantly localized in the mitochondria, reduces methionine-\n                      <jats:italic toggle=\"yes\">S<\/jats:italic>\n                      -sulfoxide, scavenging reactive oxygen species (ROS). Cisplatin, an anticancer drug, accumulates at high levels in the mitochondria of renal cells, causing mitochondrial impairment that ultimately leads to nephrotoxicity. Here, we investigated the role of MsrA in cisplatin-induced mitochondrial damage and kidney cell death using\n                      <jats:italic toggle=\"yes\">MsrA<\/jats:italic>\n                      gene-deleted (\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      <\/jats:italic>\n                      ) mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Cisplatin injection resulted in increases of ROS production, methionine oxidation, and oxidative damage in the kidneys. This oxidative stress was greater in\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      <\/jats:italic>\n                      mouse kidneys than in wild-type (\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>+\/+<\/jats:sup>\n                      <\/jats:italic>\n                      ) mouse kidneys.\n                      <jats:italic toggle=\"yes\">MsrA<\/jats:italic>\n                      gene deletion exacerbated cisplatin-induced reductions in the expression and activity of MsrA and MsrBs, and the expression of thioredoxin 1, glutathione peroxidase 1 and 4, mitochondrial superoxide dismutase, cystathionine-\u03b2-synthase, and cystathionine-\u03b3-lyase. Cisplatin induced swelling, cristae loss, and fragmentation of mitochondria with increased lipid peroxidation, more so in\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      <\/jats:italic>\n                      than in\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>+\/+<\/jats:sup>\n                      <\/jats:italic>\n                      kidneys. The ratio of mitochondrial fission regulator (Fis1) to fusion regulator (Opa1) was higher in\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      <\/jats:italic>\n                      than\n                      <jats:italic toggle=\"yes\">\n                        MsrA\n                        <jats:sup>+\/+<\/jats:sup>\n                      <\/jats:italic>\n                      mice.\n                      <jats:italic toggle=\"yes\">MsrA<\/jats:italic>\n                      deletion exacerbated cisplatin-induced increases in Bax to Bcl-2 ratio, cleaved caspase-3 level, and apoptosis, whereas MsrA overexpression attenuated cisplatin-induced oxidative stress and apoptosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation:<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">MsrA<\/jats:italic>\n                      gene deletion in mice exacerbates cisplatin-induced renal injury through increases of mitochondrial susceptibility, whereas MsrA overexpression protects cells against cisplatin.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      This study demonstrates that MsrA protects kidney cells against cisplatin-induced methionine oxidation, oxidative stress, mitochondrial damage, and apoptosis, suggesting that MsrA could be a useful target protein for the treatment of cisplatin-induced nephrotoxicity.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      27, 727\u2013741.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2016.6874","type":"journal-article","created":{"date-parts":[[2017,2,4]],"date-time":"2017-02-04T01:44:00Z","timestamp":1486172640000},"page":"727-741","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":34,"title":["Methionine Sulfoxide Reductase A Deficiency Exacerbates Cisplatin-Induced Nephrotoxicity\n                    <i>via<\/i>\n                    Increased Mitochondrial Damage and Renal Cell Death"],"prefix":"10.1177","volume":"27","author":[{"given":"Mi Ra","family":"Noh","sequence":"first","affiliation":[{"name":"Kyungpook National University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ki Young","family":"Kim","sequence":"additional","affiliation":[{"name":"Yeungnam University College of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang Jun","family":"Han","sequence":"additional","affiliation":[{"name":"Kyungpook National University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jee In","family":"Kim","sequence":"additional","affiliation":[{"name":"Keimyung University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hwa-Young","family":"Kim","sequence":"additional","affiliation":[{"name":"Yeungnam University College of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kwon Moo","family":"Park","sequence":"additional","affiliation":[{"name":"Kyungpook National University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,10,10]]},"reference":[{"key":"e_1_3_3_2_2","first-page":"121","article-title":"Hydrogen sulfide ameliorates the kidney dysfunction and damage in cisplatin-induced nephrotoxicity in rat","volume":"5","author":"Ahangarpour A","year":"2014","unstructured":"Ahangarpour A, , Abdollahzade Fard A, , Gharibnaseri MK, , Jalali T, , and Rashidi I. 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