{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T19:31:52Z","timestamp":1776108712672,"version":"3.50.1"},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,11,26]],"date-time":"2021-11-26T00:00:00Z","timestamp":1637884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Wound Repair Regeneration"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Wound healing may be disrupted by lipopolysaccharide (LPS)\u2010induced mitochondrial dysfunction, inflammation, and excessive oxidative stress, which can lead to undesirable consequences. The haematopoietic cell\u2010specific protein 1\u2010associated protein X\u20101 (HAX\u20101) is a mitochondrial matrix protein that regulates mitochondrial function. This study aimed to comprehensively identify the role of <jats:italic>HAX\u20101<\/jats:italic> in the inhibition of LPS\u2010induced mitochondrial dysfunction and apoptosis in human dermal fibroblasts (HDFs). HAX\u20101 expression was assessed in the HDF\u2010a cell line using real\u2010time polymerase chain reaction, western blotting, and immunohistochemical staining. The viability, migration, and apoptosis of HDF\u2010a cells were evaluated using the water\u2010soluble tetrazolium\u20101 assay, transwell assay, and flow cytometry analysis, respectively. Mitochondrial function was evaluated based on reactive oxygen species (ROS) generation and mitochondrial membrane potential (\u0394\u03a8<jats:italic>m<\/jats:italic>). Our results demonstrated that LPS stimulation markedly repressed <jats:italic>HAX\u20101<\/jats:italic> expression in HDFs and silencing of <jats:italic>HAX\u20101<\/jats:italic> led to mitochondrial ROS accumulation, \u0394\u03a8<jats:italic>m<\/jats:italic> disruption, and abnormal mitochondrial morphology. Accordingly, overexpression of <jats:italic>HAX\u20101<\/jats:italic> or administration of metformin enhanced mitochondrial fusion and normalized mitochondrial dynamics, thereby reversing LPS\u2010induced mitochondrial dysfunction, fibroblast apoptosis, and viability and migration inhibition in HDF\u2010a cells. These data support a mechanism wherein HAX\u20101 plays a crucial role in LPS\u2010induced fibroblast apoptosis in a mitochondria\u2010dependent manner.<\/jats:p>","DOI":"10.1111\/wrr.12985","type":"journal-article","created":{"date-parts":[[2021,11,26]],"date-time":"2021-11-26T19:34:54Z","timestamp":1637955294000},"page":"34-44","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Role of haematopoietic <scp>cell\u2010specific<\/scp> protein <scp>1\u2010associated<\/scp> protein X\u20101 gene in <scp>lipopolysaccharide\u2010induced<\/scp> apoptosis of human dermal fibroblasts"],"prefix":"10.1111","volume":"30","author":[{"given":"Mei","family":"Ning","sequence":"first","affiliation":[{"name":"Department of General Surgery Hongqi Hospital Affiliated to Mudanjiang Medical University  Mudanjiang 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