The crosstalk among TLR2, TLR4 and pathogenic pathways; a treasure trove for treatment of diabetic neuropathy.

Diabetes is correlated with organ failures as a consequence of microvascular diabetic complications, including neuropathy, nephropathy, and retinopathy. These difficulties come with serious clinical manifestations and high medical costs. Diabetic neuropathy (DN) is one of the most prevalent diabetes complications, affecting at least 50% of diabetic patients with long disease duration. DN has serious effects on patients' life since it interferes with their daily physical activities and causes psychological comorbidities. There are some potential risk factors for the development of neuropathic injuries. It has been shown that inflammatory mechanisms play a pivotal role in the progression of DN. Among inflammatory players, TLR2 and TLR4 have gained immense importance because of their ability in recognizing distinct molecular patterns of invading pathogens and also damage-associated molecular patterns (DAMPs) providing inflammatory context for the progression of a wide array of disorders. We, therefore, sought to explore the possible role of TLR2 and TLR4 in DN pathogenesis and if whether manipulating TLRs is likely to be successful in fighting off DN.