{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:10:18Z","timestamp":1787008218434,"version":"build-2736575974"},"reference-count":75,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2018,7,1]],"date-time":"2018-07-01T00:00:00Z","timestamp":1530403200000},"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":[[2018,7]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>\n                      Muscle damage in Duchenne muscular dystrophy (DMD) caused by the lack of dystrophin is strongly linked to inflammation. Heme oxygenase-1 (HO-1;\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      ) is an anti-inflammatory and cytoprotective enzyme affecting myoblast differentiation by inhibiting myomiRs. The role of HO-1 has not been so far well addressed in DMD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      In dystrophin-deficient\n                      <jats:italic toggle=\"yes\">mdx<\/jats:italic>\n                      mice, expression of\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      in limb skeletal muscles and diaphragm is higher than in wild-type animals, being consistently elevated from 8 up to 52 weeks, both in myofibers and inflammatory leukocytes. Accordingly, HO-1 expression is induced in muscles of DMD patients. Pharmacological inhibition of HO-1 activity or genetic ablation of\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      aggravates muscle damage and inflammation in\n                      <jats:italic toggle=\"yes\">mdx<\/jats:italic>\n                      mice. Double knockout animals (\n                      <jats:italic toggle=\"yes\">\n                        Hmox1\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                        mdx)\n                      <\/jats:italic>\n                      demonstrate impaired exercise capacity in comparison with\n                      <jats:italic toggle=\"yes\">mdx<\/jats:italic>\n                      mice. Interestingly, in contrast to the effect observed in muscle fibers, in dystrophin-deficient muscle satellite cells (SCs) expression of\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      is decreased, while MyoD, myogenin, and miR-206 are upregulated compared with wild-type counterparts.\n                      <jats:italic toggle=\"yes\">Mdx<\/jats:italic>\n                      SCs demonstrate disturbed and enhanced differentiation, which is further intensified by\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      deficiency. RNA sequencing revealed downregulation of Atf3, MafK, Foxo1, and Klf2 transcription factors, known to activate\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      expression, as well as attenuation of nitric oxide-mediated cGMP-dependent signaling in\n                      <jats:italic toggle=\"yes\">mdx<\/jats:italic>\n                      SCs. Accordingly, treatment with NO-donor induces\n                      <jats:italic toggle=\"yes\">Hmox1<\/jats:italic>\n                      expression and inhibits differentiation. Finally, differentiation of\n                      <jats:italic toggle=\"yes\">mdx<\/jats:italic>\n                      SCs was normalized by CO, a product of HO-1 activity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation and Conclusions:<\/jats:title>\n                    <jats:p>\n                      HO-1 is induced in DMD, and HO-1 inhibition aggravates DMD pathology. Therefore, HO-1 can be considered a therapeutic target to alleviate this disease.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal<\/jats:italic>\n                      . 29, 128\u2013148.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2017.7435","type":"journal-article","created":{"date-parts":[[2018,4,19]],"date-time":"2018-04-19T05:01:39Z","timestamp":1524114099000},"page":"128-148","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":45,"title":["Heme Oxygenase-1 Influences Satellite Cells and Progression of Duchenne Muscular Dystrophy in Mice"],"prefix":"10.1177","volume":"29","author":[{"given":"Katarzyna","family":"Pietraszek-Gremplewicz","sequence":"first","affiliation":[{"name":"Jagiellonian University","place":["Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Kozakowska","sequence":"additional","affiliation":[{"name":"Jagiellonian 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