Engineering stem cell exosomes promotes the survival of multi-territory perforator flap in diabetes via regulating anti-inflammatory and angiogenesis

微泡 血管生成 干细胞 炎症 糖尿病 细胞生物学 组织修复 医学 癌症研究 免疫学 生物 小RNA 内分泌学 生物化学 基因
作者
Chao Sun,Junwei Su,Zheng Wang,Changjiang Liu,Xinzeyu Yi,Weimin Chen,Dong Zhang,Aixi Yu
出处
期刊:Regenerative Biomaterials [University of Oxford]
卷期号:12: rbaf075-rbaf075
标识
DOI:10.1093/rb/rbaf075
摘要

Abstract The versatile multi-territory perforator flap remains a cornerstone of reconstructive surgery for diabetic ulcerations, yet its clinical efficacy faces significant challenges in hyperglycemic conditions. The diabetic milieu significantly exacerbates tissue ischemia through augmented chronic inflammation and impaired angiogenesis, which collectively harm flap perfusion and compromise its overall viability. A major postoperative complication is distal flap necrosis, which is closely associated with the critical “Choke zone,” a hypoperfused transitional area that exhibits delayed vascular recruitment and suboptimal angiogenesis. This vascular bottleneck creates a precarious balance between tissue oxygen demand and supply, ultimately compromising flap viability. To address this issue, we have developed the engineering stem cell exosomes by encapsulating metformin-loaded Mesoporous silica nanoparticles into BMSC exosomes (M-MS@EXO NPs), enabling the release of metformin. Compared to traditional oral medication, delivering metformin through engineered exosomes allows for precise administration in diabetic wounds. The multifunctional M-MS@EXO NPs exhibit dual pharmacological activity by reducing the secretion of inflammatory cytokines while effectively remodeling the vascular niche within the diabetic microenvironment. Additionally, the M-MS@EXO NPs show anti-inflammatory and angiogenesis effects by inhibiting TNF/apoptosis and enhancing VEGF signaling pathways in vitro. In the dorsal multi-territory perforator flap model of type 2 diabetes, the M-MS@EXO NPs demonstrate the ability to alleviate inflammation and promote neovascularization of the Choke zone, reducing distal necrosis, which holds great promise for improving flap survival in diabetes.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
vva发布了新的文献求助10
刚刚
刚刚
小二郎的应助被YL采纳,获得10
1秒前
徐徐发布了新的文献求助10
1秒前
1秒前
1秒前
1秒前
1秒前
2秒前
2秒前
思源的应助被安静的毛衣采纳,获得10
2秒前
2秒前
2秒前
2秒前
2秒前
2秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
3秒前
4秒前
4秒前
4秒前
4秒前
4秒前
4秒前
4秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Organizational Behavior 510
A Silent Apostrophe:The Fayum Portraits 350
Sing with Understanding: Introduction to Theology in Christian Congregational Song, 3rd ed 330
Auslegung und Untersuchung einer invers ausgelegten Beschaufelung eines einstufigen Axialverdichters mit Vorleitrad (German) 300
AI-Contracting 300
四川大学学位论文.郭瑞昂. 基于高压热扩散的n型磷掺杂金刚石半导体制备研究 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 有机化学 化学工程 内科学 物理 生物化学 复合材料 催化作用 细胞生物学 人工智能 心理学 无机化学 基因 遗传学
热门帖子
关注 科研通微信公众号,转发送积分 7839932
求助须知:如何正确求助?哪些是违规求助? 9361832
关于积分的说明 20622819
捐赠科研通 7434496
什么是DOI,文献DOI怎么找? 3339432
关于科研通互助平台的介绍 2483808
邀请新用户注册赠送积分活动 2361041