Unveiling the crucial role of intercellular adhesion molecule-1 in secondary diabetic complications.
Prabhnain KaurRitu DahiyaMukesh NandaveKalicharan SharmaRamesh K GoyalPublished in: Cell biochemistry and function (2024)
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.
Keyphrases
- oxidative stress
- type diabetes
- diabetic retinopathy
- risk factors
- cardiovascular disease
- mental health
- wound healing
- healthcare
- dna damage
- heart failure
- public health
- systematic review
- glycemic control
- cell adhesion
- biofilm formation
- stem cells
- metabolic syndrome
- diabetic rats
- randomized controlled trial
- risk assessment
- skeletal muscle
- signaling pathway
- optical coherence tomography
- induced apoptosis
- cystic fibrosis
- atrial fibrillation
- cell migration
- heat shock protein
- drug induced
- replacement therapy