ArticleJournal of orthopaedic surgery and research2025
Upregulation of lncRNA SSTR5-AS1 promotes osteoblast differentiation and reduces apoptosis.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveOsteoporotic fractures (OPF) and delayed fracture healing (DFH) pose major health challenges for the elderly. The lncRNA SSTR5-AS1 shows abnormal expression in people with low BMD. Understanding how SSTR5-AS1 regulates fracture healing could help address DFH.
methodsThis study detected the expression levels of SSTR5-AS1, miR-193b-3p, osteogenic markers (RUNX2, ALP, BSP, OCN, OPN) mRNA, and apoptosis-related genes (Bcl-2, Bax, Bad) in osteoblasts and serum samples from all participants using RT-qPCR. Logistic regression was used to identify the independent factors influencing fracture healing. Cell proliferation and apoptosis were assessed using CCK-8 assays and flow cytometry, respectively. The binding relationship between SSTR5-AS1 and miR-193b-3p was validated through dual-luciferase reporter assays.
resultsSSTR5-AS1 is significantly downregulated in patients with OPF and DFH and negatively regulates the expression level of miR-193b-3p. SSTR5-AS1 is a protective factor for fracture healing. Elevating SSTR5-AS1 levels significantly reduces miR-193b-3p expression, thereby decreasing osteoblast apoptosis, increasing Bcl-2 expression, and decreasing Bax and Bad levels. Furthermore, enhancing SSTR5-AS1 promotes osteoblast proliferation, upregulates RUNX2, ALP, BSP, OCN, and OPN expression, and facilitates osteoblast differentiation.
conclusionSSTR5-AS1 demonstrates significant diagnostic value for OPF and DFH, making it a promising biomarker for these conditions. When overexpressed, SSTR5-AS1 reduces miR-193b-3p levels, promoting osteoblast proliferation and differentiation. This may accelerate fracture healing.
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