Azka Khan
In biomedical research, the discovery and validation of drug targets are essential, and numerous studies have been done to analyse drug target properties in order to better understand the fundamentals of their actions. However, the majority of them are based on either solid biological assumptions or the distinct chemical and physical characteristics of those targets. In this study, we evaluated three major approaches to understanding functional biomolecules based on the topological characteristics of pharmacological targets. The protein-protein interactions network shows no discernible distinctions between targets and common proteins, indicating the drug targets are neither the bridge proteins nor the dominating hub proteins. There are notable distinctions between known targets and other proteins based on some unique topological structures of the pharmacological targets. There are notable distinctions between the known targets and other proteins based on certain unique topological structures of the pharmacological targets. Additionally, based on their modularity, the pharmacological targets primarily belong to three types of communities. These topological characteristics can be used to better understand how the PPI network's drug targets function. In particular, it is a different approach to extract no targets or anticipate possible targets to test a new therapeutic target quickly and affordably. In this manner, the homologous set of a pharmacological target, which contains 102 possible target proteins, is predicted in the article.
People with diabetic nephropathy (DN) have a lower quality of life and a shorter life expectancy. Evidence suggests that interactions between activated protein kinase C (PKC), advanced glycation end products (AGEs), and angiotensin II worsen the course of DN. A number of drugs have been studied to see if they can reduce the progression of DN, including AGEs, PKC, renin-angiotensin-aldosterone system (RAAS), and angiotensin-converting enzyme (ACEI) inhibitors. It is unclear whether specific molecular targets of drugs cause an improvement in renal damage in DN. In this review, the prospective treatment targets are outlined based on hypothesised illness progression mechanisms.
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