{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:03:27Z","timestamp":1792785807139,"version":"4.5.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T00:00:00Z","timestamp":1717113600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100011960","name":"DEBRA International","doi-asserted-by":"publisher","award":["Castiglia-1 to D"],"award-info":[{"award-number":["Castiglia-1 to D"]}],"id":[{"id":"10.13039\/501100011960","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004726","name":"Ministry of Health","doi-asserted-by":"publisher","award":["RF-2021-12372117"],"award-info":[{"award-number":["RF-2021-12372117"]}],"id":[{"id":"10.13039\/501100004726","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Canton"},{"DOI":"10.13039\/501100005869","name":"University of Fribourg","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005869","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,9,18]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Recessive dystrophic epidermolysis bullosa (RDEB) is a blistering disease caused by mutations in the gene encoding type VII collagen (C7). RDEB is associated with fibrosis, which is responsible for severe complications. The phenotypic variability observed in siblings with RDEB suggests that epigenetic modifications contribute to disease severity. Identifying epigenetic changes may help to uncover molecular mechanisms underlying RDEB pathogenesis and new therapeutic targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To investigate histone acetylation in RDEB skin and to explore histone deacetylase inhibitors (HDACi) as therapeutic molecules capable of counteracting fibrosis and disease progression in RDEB mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Acetylated histone levels were detected in human skin by immunofluorescence and in RDEB fibroblasts by enzyme-linked immunosorbent assay (ELISA). The effects of givinostat and valproic acid (VPA) on RDEB fibroblast fibrotic behaviour were assessed by a collagen\u2013gel contraction assay, Western blot and immunocytofluorescence for \u03b1-smooth muscle actin, and ELISA for released transforming growth factor (TGF)-\u03b21. RNA sequencing was performed in HDACi- and vehicle-treated RDEB fibroblasts. VPA was systemically administered to RDEB mice and effects on overt phenotype were monitored. Fibrosis was investigated in the skin using histological and immunofluorescence analyses. Eye and tongue defects were examined microscopically. Mass spectrometry proteomics was performed on skin protein extracts from VPA-treated RDEB and control mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Histone acetylation decreases in RDEB skin and primary fibroblasts. RDEB fibroblasts treated with HDACi lowered fibrotic traits, including contractility, TGF-\u03b21 release and proliferation. VPA administration to RDEB mice mitigated severe manifestations affecting the eyes and paws. These effects were associated with fibrosis inhibition. Proteomic analysis of mouse skin revealed that VPA almost normalized protein sets involved in protein synthesis and immune response, processes linked to the increased susceptibility to cancer and bacterial infections seen in people with RDEB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Dysregulated histone acetylation contributes to RDEB pathogenesis by facilitating the progression of fibrosis. Repurposing of HDACi could be considered for disease-modifying treatments in RDEB.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/bjd\/ljae225","type":"journal-article","created":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T18:20:58Z","timestamp":1717179658000},"page":"568-579","source":"Crossref","is-referenced-by-count":13,"title":["Histone deacetylase inhibition mitigates fibrosis-driven\u00a0disease progression in recessive dystrophic\u00a0epidermolysis bullosa"],"prefix":"10.1093","volume":"191","author":[{"given":"Alessia","family":"Primerano","sequence":"first","affiliation":[{"name":"Laboratory of Molecular and Cell Biology, IDI-IRCCS , Rome ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emanuela","family":"De Domenico","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cell Biology, IDI-IRCCS , Rome 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