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In this study, we explored whether endogenous gasotransmitter hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) could protect against DOX\u2010induced cardiomyocyte apoptosis and its mechanisms. The results indicated that DOX significantly downregulated endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S production and endogenous synthetase cystathionine\n                    <jats:italic>\u03b3<\/jats:italic>\n                    \u2010lyase (CSE) expression and obviously stimulated the apoptosis in H9C2 cells. The supplement of H\n                    <jats:sub>2<\/jats:sub>\n                    S donor sodium hydrosulfide (NaHS) or overexpression of CSE inhibited DOX\u2010induced H9C2 cell apoptosis. DOX enhanced the activities of caspase family members in cardiomyocytes, while NaHS attenuated DOX\u2010enhanced caspase\u20103, caspase\u20102, and caspase\u20109 activities by 223.1%, 73.94%, and 52.29%, respectively. Therefore, taking caspase\u20103 as a main target, we demonstrated that NaHS or CSE overexpression alleviated the cleavage of caspase\u20103, suppressed caspase\u20103 activity, and inhibited the cleavage of poly ADP\u2010ribose polymerase (PARP). Mechanistically, we found that H\n                    <jats:sub>2<\/jats:sub>\n                    S persulfidated caspase\u20103 in H9C2 cells and human recombinant caspase\u20103 protein, while the thiol\u2010reducing agent dithiothreitol (DTT) abolished H\n                    <jats:sub>2<\/jats:sub>\n                    S\u2010induced persulfidation of caspase\u20103 and thereby prevented the antiapoptotic effect of H\n                    <jats:sub>2<\/jats:sub>\n                    S on caspase\u20103 in H9C2 cells. The mutation of caspase\u20103 C148S and C170S failed to block caspase\u20103 persulfidation by H\n                    <jats:sub>2<\/jats:sub>\n                    S in H9C2 cells. However, caspase\u20103 C163S mutation successfully abolished the effect of H\n                    <jats:sub>2<\/jats:sub>\n                    S on caspase\u20103 persulfidation and the corresponding protection of H9C2 cells. Collectively, these findings indicate that endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S persulfidates caspase\u20103 at cysteine 163, inhibiting its activity and cardiomyocyte apoptosis. Sufficient endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S might be necessary for the protection against myocardial cell apoptosis induced by DOX. The results of the study might open new avenues with respect to the therapy of DOX\u2010stimulated cardiomyopathy.\n                  <\/jats:p>","DOI":"10.1155\/2022\/6153772","type":"journal-article","created":{"date-parts":[[2022,5,4]],"date-time":"2022-05-04T20:50:09Z","timestamp":1651697409000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Endogenous Hydrogen Sulfide Persulfidates Caspase\u20103 at Cysteine 163 to Inhibit Doxorubicin\u2010Induced Cardiomyocyte Apoptosis"],"prefix":"10.1155","volume":"2022","author":[{"given":"Xiaoyun","family":"Ye","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingying","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Boyang","family":"Lv","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingquan","family":"Qiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shangyue","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanlin","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Kong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chaoshu","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaqian","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junbao","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1606-8988","authenticated-orcid":false,"given":"Hongfang","family":"Jin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2022,5,4]]},"reference":[{"key":"e_1_2_10_1_2","doi-asserted-by":"publisher","DOI":"10.1002\/cncr.11407"},{"key":"e_1_2_10_2_2","doi-asserted-by":"publisher","DOI":"10.1159\/000265166"},{"key":"e_1_2_10_3_2","doi-asserted-by":"publisher","DOI":"10.1124\/mol.119.115725"},{"key":"e_1_2_10_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0300-483X(94)02867-T"},{"key":"e_1_2_10_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2919"},{"key":"e_1_2_10_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.toxlet.2019.02.013"},{"key":"e_1_2_10_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.2042-7158.1986.tb04566.x"},{"key":"e_1_2_10_8_2","doi-asserted-by":"publisher","DOI":"10.2147\/JIR.S304520"},{"key":"e_1_2_10_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.119.314681"},{"key":"e_1_2_10_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2019.108238"},{"key":"e_1_2_10_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2017.05.003"},{"key":"e_1_2_10_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jelectrocard.2019.02.009"},{"key":"e_1_2_10_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400601"},{"key":"e_1_2_10_14_2","doi-asserted-by":"publisher","DOI":"10.1038\/cdd.2009.29"},{"key":"e_1_2_10_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2017.09.001"},{"key":"e_1_2_10_16_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1745-7270.2005.00108.x"},{"key":"e_1_2_10_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbi.2019.03.027"},{"key":"e_1_2_10_18_2","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2006.0161"},{"key":"e_1_2_10_19_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.102.5.572"},{"key":"e_1_2_10_20_2","doi-asserted-by":"publisher","DOI":"10.1038\/srep44735"},{"key":"e_1_2_10_21_2","doi-asserted-by":"publisher","DOI":"10.1111\/imr.12541"},{"key":"e_1_2_10_22_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10495-016-1247-0"},{"key":"e_1_2_10_23_2","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1005"},{"key":"e_1_2_10_24_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.282.5392.1318"},{"key":"e_1_2_10_25_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41420-018-0062-5"},{"key":"e_1_2_10_26_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2008.02.026"},{"key":"e_1_2_10_27_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-03-01066.1996"},{"key":"e_1_2_10_28_2","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0211hyp"},{"key":"e_1_2_10_29_2","article-title":"Hydrogen sulfide as a messenger molecule in cardiovascular system","volume":"34","author":"Du J. 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