Nanomedicine for the treatment of diabetes-associated cardiovascular diseases and fibrosis.

Cardiomyopathy and fibrosis are the main causes of heart failure in diabetes patients. For therapeutic purposes, a delivery system is required to enhance antidiabetic drug efficacy and specifically target profibrotic pathways in cardiomyocytes. Nanoparticles (NPs) have distinct advantages, including biocompatibility, bioavailability, targeting efficiency, and minimal toxicity, which make them ideal for antidiabetic treatment. In this review, we overview the latest information on the pathogenesis of cardiomyopathy and fibrosis in diabetes patients. We summarize how NP applications improve insulin and liraglutide efficacy and their sustained release upon oral administration. We provide a comprehensive review of the results of NP clinical trials in diabetes patients and of animal studies investigating the effects of NP-mediated anti-fibrotic treatments. Collectively, the application of advanced NP delivery systems in the treatment of cardiomyopathy and fibrosis in diabetes patients is a promising and innovative therapeutic strategy. Conventional anti-diabetic regimens are challenged by the drug's efficacy, weak potency in the protection from cardiomyopathy and suppression of cardiac fibrosis progression. Nanoparticles hold distinguished advantaged such as biocompatibility, water solubility, bioavailability, target efficiency and minimized toxicity, all of which make them ideal for drug, nucleic acid and protein delivery in anti-diabetic treatment. For the therapeutic purposes, the desirable NPs delivery system should be safe with well-controlled drug retention and release and bioavailability. Lipid- and chemical- modified nanoparticles make it possible for oral administration of insulin and GLP-1 RAs in diabetic patients with sustained release and stable reduction of HbA1c. NPs are designed and desirable to deliver nucleic acids, small molecules or peptides specifically to the heart where they block TGF-β1 activation in fibroblasts and cell type transition from epithelial to fibroblasts, resulting in the inhibition of cardiac fibrosis progression. [Display omitted] [ABSTRACT FROM AUTHOR]