{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T22:25:26Z","timestamp":1790893526945,"version":"4.1.0"},"reference-count":75,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"669","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2022,11,2]]},"abstract":"<jats:p>\n            Immune checkpoint inhibitors (ICIs) have been increasingly used in combination for cancer treatment but are associated with myocarditis. Here, we report that tumor-bearing mice exhibited response to treatment with combinatorial anti\u2013programmed cell death 1 and anti\u2013cytotoxic T lymphocyte antigen\u20134 antibodies but also presented with cardiovascular toxicities observed clinically with ICI therapy, including myocarditis and arrhythmia. Female mice were preferentially affected with myocarditis compared to male mice, consistent with a previously described genetic model of ICI myocarditis and emerging clinical data. Mechanistically, myocardial tissue from ICI-treated mice, the genetic mouse model, and human heart tissue from affected patients with ICI myocarditis all exhibited down-regulation of\n            <jats:italic>MANF<\/jats:italic>\n            (mesencephalic astrocyte\u2013derived neurotrophic factor) and\n            <jats:italic>HSPA5<\/jats:italic>\n            (heat shock 70-kDa protein 5) in the heart; this down-regulation was particularly notable in female mice. ICI myocarditis was amplified by heart-specific genetic deletion of mouse\n            <jats:italic>Manf<\/jats:italic>\n            and was attenuated by administration of recombinant MANF protein, suggesting a causal role. Ironically, both\n            <jats:italic>MANF<\/jats:italic>\n            and\n            <jats:italic>HSPA5<\/jats:italic>\n            were transcriptionally induced by liganded estrogen receptor \u03b2 and inhibited by androgen receptor. However, ICI treatment reduced serum estradiol concentration to a greater extent in female compared to male mice. Treatment with an estrogen receptor \u03b2\u2013specific agonist and androgen depletion therapy attenuated ICI-associated cardiac effects. Together, our data suggest that ICI treatment inhibits estradiol-dependent expression of\n            <jats:italic>MANF\/HSPA5<\/jats:italic>\n            in the heart, curtailing the cardiomyocyte response to immune injury. This endocrine-cardiac-immune pathway offers new insights into the mechanisms of sex differences in cardiac disease and may offer treatment strategies for ICI myocarditis.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.abo1981","type":"journal-article","created":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T17:58:46Z","timestamp":1667411926000},"source":"Crossref","is-referenced-by-count":65,"title":["Hormonal therapies up-regulate MANF and overcome female susceptibility to immune checkpoint inhibitor myocarditis"],"prefix":"10.1126","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9741-591X","authenticated-orcid":true,"given":"Yaohua","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA."},{"name":"Beijing Institute of Brain Disorders, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing 10069, 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