Sandhanam K, Bhattacharjee Bedanta, Rynjah Damanbhalang, Kalita Pratap, Sen Saikat, Chakraborty Raja
Department of Pharmacology, KMCH College of Pharmacy, Coimbatore, 641048, Tamil Nadu, India.
School of Pharmaceutical Sciences, Girijananda Chowdhury University-Tezpur Campus, 784501, Assam, India.
Curr Diabetes Rev. 2024 Nov 29. doi: 10.2174/0115733998335873241012161428.
Diabetic chronic wounds and amputations are very serious complications of diabetes mellitus (DM) that result from an integration factor, including oxygen deprivation, elevated reactive oxygen species (ROS), reduced angiogenesis, and microbial invasion. These causative factors lead to tenacious wounds in an inflammatory state, which eventually results in tissue aging and necrosis. Wound healing in DM potentially targets C-X-C chemokine receptor type 4 (CXCR4) regulates several signalling pathways. The CXCR4 signalling pathway integrated with phospholipase C (PLC)/protein kinase-C (PKC) Ca2+ pathways, stromal cell-derived factor-1 (SDF-1), and mitogen- activated protein kinases (MAPKs) pathway for enhancing cell chemotaxis, proliferation, and survival. The dysregulated CXCR4 pathway is connected with poor wound healing in DM patients. Therapeutic strategies targeting CXCR4-based molecules such as UCUF-728, UCUF-965, and AMD3100 have been shown to enhance diabetic wound healing by altering miRNA expression, promoting angiogenesis, and accelerating wound closure. This study indicates that CXCR4 participation in various signalling pathways makes it essential for Understanding the healing of diabetic wounds. Using specific compounds to target CXCR4 offers a potentially effective treatment strategy to improve wound healing in diabetes. Our understanding of CXCR4 signalling and its regulation processes will enable us to develop more potent wound care solutions for diabetic chronic wounds. This report concludes that CXCR4's potential therapeutic targeting shows improvements in diabetic wound repair. This review will demonstrate that CXCR4 plays a major role in wound healing through its various signalling pathways. Targeting CXCR4 with certain agonist molecules shows a therapeutic approach to potentially increasing wound healing in diabetes. By enhancing our understanding of the CXCR4 signalling mechanism in future studies, we can develop more potential treatments for chronic diabetic wounds.
糖尿病慢性伤口和截肢是糖尿病(DM)非常严重的并发症,其由多种因素共同作用导致,包括缺氧、活性氧(ROS)升高、血管生成减少和微生物入侵。这些致病因素导致伤口处于炎症状态且难以愈合,最终导致组织衰老和坏死。糖尿病患者伤口愈合可能靶向C-X-C趋化因子受体4(CXCR4),其调节多种信号通路。CXCR4信号通路与磷脂酶C(PLC)/蛋白激酶C(PKC)Ca2+通路、基质细胞衍生因子-1(SDF-1)和丝裂原活化蛋白激酶(MAPKs)通路整合,以增强细胞趋化性、增殖和存活。CXCR4通路失调与糖尿病患者伤口愈合不良有关。针对基于CXCR4的分子(如UCUF-728、UCUF-965和AMD3100)的治疗策略已显示可通过改变miRNA表达、促进血管生成和加速伤口闭合来促进糖尿病伤口愈合。本研究表明,CXCR4参与各种信号通路使其对于理解糖尿病伤口愈合至关重要。使用特定化合物靶向CXCR4提供了一种潜在有效的治疗策略,以改善糖尿病患者的伤口愈合。我们对CXCR4信号及其调节过程的理解将使我们能够为糖尿病慢性伤口开发更有效的伤口护理解决方案。本报告得出结论,CXCR4的潜在治疗靶向显示出糖尿病伤口修复有所改善。本综述将证明CXCR4通过其各种信号通路在伤口愈合中起主要作用。用某些激动剂分子靶向CXCR4显示出一种可能增加糖尿病患者伤口愈合率的治疗方法。通过在未来研究中加强我们对CXCR4信号机制的理解,我们可以为慢性糖尿病伤口开发更多潜在治疗方法。