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SFRP2 调节糖尿病伤口愈合过程中巨噬细胞功能表型转化和能量代谢。

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing.

机构信息

Institute of Plastic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

Clinical Research Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

出版信息

Front Immunol. 2024 Oct 11;15:1432402. doi: 10.3389/fimmu.2024.1432402. eCollection 2024.

DOI:10.3389/fimmu.2024.1432402
PMID:39464880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11502328/
Abstract

Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood. We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, but did not affect wound healing process of control mice. In addition, suppression of SFRP2 increased macrophage infiltration and impeded the transition of macrophages functional phenotypes during diabetic wound healing, and affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages, but impeded both glycolysis and mitochondrial energy metabolism in inflammatory macrophages. In addition, suppression of SFRP2 inhibited wnt signaling-related genes in macrophages. Treatment of AAV-SFRP2 augmented wound healing in diabetic mice and demonstrated the therapeutic potential of SFRP2. In conclusions, SFRP2 may function as a wound healing-related gene in DFU by modulating functional phenotype transition of macrophages and the balance between mitochondrial energy metabolism and glycolysis.

摘要

糖尿病足溃疡（DFU）是糖尿病的一种严重并发症，给患者的健康带来了极大的损害，并造成了沉重的经济负担。DFU 的发病机制尚未完全阐明。我们利用生物信息学分析筛选了与伤口愈合相关的基因，并利用全层皮肤损伤小鼠模型和细胞实验来探讨这些靶基因在糖尿病伤口愈合中的作用。SFRP2 被鉴定为与伤口愈合相关的基因，其表达与 DFU 中的免疫细胞浸润有关。研究表明，SFRP2 的抑制延迟了糖尿病小鼠的伤口愈合过程，阻碍了血管生成和基质重塑，但对对照小鼠的伤口愈合过程没有影响。此外，SFRP2 的抑制增加了巨噬细胞的浸润，并阻碍了糖尿病伤口愈合过程中巨噬细胞功能表型的转变，影响了伤口愈合早期与炎症反应和能量代谢相关的转录组特征。细胞外通量分析（EFA）显示，SFRP2 的抑制降低了损伤相关巨噬细胞中的线粒体能量代谢和糖酵解，但阻碍了炎症巨噬细胞中的糖酵解和线粒体能量代谢。此外，SFRP2 的抑制抑制了巨噬细胞中的 Wnt 信号相关基因。AAV-SFRP2 的治疗增强了糖尿病小鼠的伤口愈合，并证明了 SFRP2 的治疗潜力。总之，SFRP2 可能通过调节巨噬细胞功能表型的转变以及线粒体能量代谢和糖酵解之间的平衡，在 DFU 中发挥与伤口愈合相关的基因作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/68f93a5fcfb5/fimmu-15-1432402-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/ba8cccf615c8/fimmu-15-1432402-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/3faf2a583724/fimmu-15-1432402-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/bf7cecde5c64/fimmu-15-1432402-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/5287e4a62d17/fimmu-15-1432402-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/11502328/68f93a5fcfb5/fimmu-15-1432402-g009.jpg

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本文引用的文献

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Mol Med Rep. 2024 Apr;29(4). doi: 10.3892/mmr.2024.13190. Epub 2024 Mar 1.
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Identifying Explainable Machine Learning Models and a Novel SFRP2 Fibroblast Signature as Predictors for Precision Medicine in Ovarian Cancer.鉴定可解释的机器学习模型和新型 SFRP2 成纤维细胞特征作为卵巢癌精准医疗的预测因子。
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regulates the WNT/β-catenin pathway to slow the development of aldosterone-producing adenoma.
调节WNT/β-连环蛋白信号通路以减缓醛固酮瘤的发展。
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Diabetic Foot Ulcers: A Review.糖尿病足溃疡：综述。
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METTL3 promotes the malignancy of non-small cell lung cancer by N6-methyladenosine modifying SFRP2.METTL3 通过 N6-甲基腺苷修饰 SFRP2 促进非小细胞肺癌的恶性转化。
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