Nutrition & diabetes · 2026
Fibrillin-1 alleviates high glucose-induced fibroblast apoptosis and inflammation via autophagy activation.
СтатьяНазвание и аннотация: Перевод в очереди
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Wang Ya, Xie Sihong, Weng Xiaoyu, Xu Cheng, Xu Shujuan
Аннотация
BACKGROUND: Effective management of fibroblast inflammation and apoptosis caused by high glucose is pivotal for mitigating diabetic foot ulcers (DFUs). Recent studies have indicated the potential involvement of Fibrillin-1 (FBN1) in DFU healing through its impact on fibroblast proliferation, migration, and apoptosis. However, detailed cellular mechanism remained uncleared.
METHODS: Three primary fibroblast cultures were established conventionally. The impact of FBN1 was studied through knockdown and overexpression. FBN1 levels were gauged via reverse transcription-quantitative polymerase chain reaction (RT-qPCR for mRNA) and Western blot (for protein). Immunofluorescence localized FBN1. Proliferation was assessed via MTT assays, and EDU staining tracked cell viability. TUNEL detected apoptosis. Inflammation was measured by ELISA. Electron microscopy visualized cellular structure changes linked to autophagy, corroborated by Western blot markers.
RESULTS: Fibroblasts exposed to high glucose exhibited dysregulated FBN1 expression and disrupted autophagy. FBN1 overexpression promoted proliferation and suppressed inflammation and apoptosis under high glucose conditions. Additionally, FBN1 was found to restore autophagy inhibited by high glucose. In contrast, FBN1 silencing further suppressed autophagy, thereby aggravating inflammation and apoptosis.
CONCLUSION: Dysregulation of FBN1 in fibroblasts induced by high glucose hampers autophagy, ultimately leading to apoptosis and inflammation. The upregulation of FBN1 counters these processes, potentially enhancing the healing of DFUs.
METHODS: Three primary fibroblast cultures were established conventionally. The impact of FBN1 was studied through knockdown and overexpression. FBN1 levels were gauged via reverse transcription-quantitative polymerase chain reaction (RT-qPCR for mRNA) and Western blot (for protein). Immunofluorescence localized FBN1. Proliferation was assessed via MTT assays, and EDU staining tracked cell viability. TUNEL detected apoptosis. Inflammation was measured by ELISA. Electron microscopy visualized cellular structure changes linked to autophagy, corroborated by Western blot markers.
RESULTS: Fibroblasts exposed to high glucose exhibited dysregulated FBN1 expression and disrupted autophagy. FBN1 overexpression promoted proliferation and suppressed inflammation and apoptosis under high glucose conditions. Additionally, FBN1 was found to restore autophagy inhibited by high glucose. In contrast, FBN1 silencing further suppressed autophagy, thereby aggravating inflammation and apoptosis.
CONCLUSION: Dysregulation of FBN1 in fibroblasts induced by high glucose hampers autophagy, ultimately leading to apoptosis and inflammation. The upregulation of FBN1 counters these processes, potentially enhancing the healing of DFUs.