{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T19:54:03Z","timestamp":1776282843526,"version":"3.50.1"},"reference-count":39,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,4,1]]},"abstract":"<jats:p>Dysfunction in key cellular organelles has been linked to diabetic complications. This study intended to investigate the alterations in the unfolded protein response (UPR), autophagy, and mitochondrial function, which are part of the endoplasmic reticulum (ER) stress response, in wound healing (WH) under diabetes conditions. WH mouse models were used to evaluate the UPR, autophagy, mitochondrial fusion, fission, and biogenesis as well as mitophagy in the skin of control and diabetic mice at baseline and 10 days after wounding. The autophagic flux in response to high-glucose conditions was also evaluated in keratinocyte and fibroblast cell cultures. WH was impaired in the diabetic mouse model, and we found that the UPR and autophagy pathways were activated in skin wounds of control mice and in the non-wounded skin of diabetic mice. Moreover, high-glucose conditions induced autophagy in the keratinocyte and fibroblast cell cultures. However, mitophagy did not change in the skin of diabetic mice or the wounded skin. In addition, mitochondrial fusion was activated in control but not in the skin wounds of diabetic mice, while mitochondrial biogenesis is downregulated in the skin of diabetic mice. In conclusion, the activation of the UPR, autophagy, and mitochondrial remodeling are crucial for a proper WH. These results suggest that the increase in ER stress and autophagy in the skin of diabetic mice at baseline significantly escalated to pathological levels after wounding, contributing to impaired WH in diabetes.<\/jats:p>","DOI":"10.1530\/jme-22-0122","type":"journal-article","created":{"date-parts":[[2023,2,3]],"date-time":"2023-02-03T16:39:01Z","timestamp":1675442341000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":9,"title":["Dysregulation of endoplasmic reticulum stress response in skin wounds in a streptozotocin-induced diabetes mouse model"],"prefix":"10.1530","volume":"70","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1748-9861","authenticated-orcid":true,"given":"Ermelindo C","family":"Leal","sequence":"first","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0168-3416","authenticated-orcid":true,"given":"Tatiana","family":"Emanuelli","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"},{"name":"Institute for Interdisciplinary Research, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9292-5961","authenticated-orcid":true,"given":"Diana","family":"Santos","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"},{"name":"Institute for Interdisciplinary Research, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7817-0881","authenticated-orcid":true,"given":"Jo\u00e3o","family":"Moura","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4660-8081","authenticated-orcid":true,"given":"Ana","family":"Catarina RG Fonseca","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8467-3840","authenticated-orcid":true,"given":"Ana","family":"Burgeiro","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6264-3632","authenticated-orcid":true,"given":"Eugenia","family":"Carvalho","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, Center for Inovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal"},{"name":"Institute for Interdisciplinary Research, University of Coimbra, Coimbra, Portugal"},{"name":"Associa\u00e7\u00e3o Protectora dos Diab\u00e9ticos de Portugal (APDP), Lisbon, Portugal"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Diabetes","first-page":"2685","article-title":"Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6","volume":"54","author":"Bach","year":"2005","unstructured":"Bach DNaon DPich SSoriano FXVega NRieusset JLaville MGuillet CBoirie YWallberg-Henriksson H2005Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6. 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