AI Article Synopsis

  • - Diabetes mellitus can lead to serious complications like diabetic retinopathy, nephropathy, and cardiomyopathy, which adversely affect patient health.
  • - Intercellular adhesion molecule-1 (ICAM-1) is related to inflammation and endothelial dysfunction, playing a significant role in the development of these diabetes-related issues.
  • - Investigating ICAM-1 could reveal new therapy options to reduce inflammation and improve blood vessel function, potentially reducing complications and improving health outcomes for diabetic patients.

Article Abstract

Diabetes mellitus is associated with secondary complications such as diabetic retinopathy (DR), nephropathy (DN), and cardiomyopathy (DCM), all of which significantly impact patient health. Intercellular adhesion molecule-1 (ICAM-1) has been implicated in inflammatory responses and endothelial dysfunction, both crucial in the pathogenesis of these complications. The goal of this review is to investigate at potential therapy methods that target ICAM-1 pathways and to better understand the multifaceted role of ICAM-1 in secondary diabetic problems. A meticulous analysis of scholarly literature published globally was conducted to examine ICAM-1involvement in inflammatory processes, endothelial dysfunction, and oxidative stress related to diabetes and its complications. Elevated ICAM-1 levels are strongly associated with augmented leukocyte adhesion, compromised microvascular function, and heightened oxidative stress in diabetes. These pathways contribute significantly to DR, DN, and DCM pathogenesis, highlighting ICAM-1 as a key player in their progression. Understanding ICAM-1 role in secondary diabetic complications offers insights into novel therapeutic strategies. Targeting ICAM-1 pathways may mitigate inflammation, improve endothelial function, and ultimately attenuate diabetic complications, thereby enhancing patient health outcomes. Continued research in this area is crucial for developing effective targeted therapies.

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http://dx.doi.org/10.1002/cbf.4037DOI Listing

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