Article Sidebar
Published:
Jan 11, 2024Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Novel approaches and therapeutic targets for diabetic nephropathy: Advances and promising strategies
Abstract
Diabetic nephropathy is a progressive condition characterized by kidney damage and functional decline, primarily attributed to hyperglycemia. Special keywords and probes related to diabetic nephropathy were utilized by Google search engine to obtain relevant information from Google, Google Scholar, PubMed, Science Alert, and Google Scholar databases. This review explores the interconnected mechanisms underlying its pathogenesis. Hyperglycemia initiates glomerular hypertrophy and increased glomerular filtration rate as compensatory responses, but persistent hyperglycemia leads to renal inflammation, oxidative stress, abnormal extracellular matrix (ECM) accumulation, and increased albuminuria. These processes contribute to structural changes, declining glomerular filtration rate, and potential end-stage renal disease (ESRD) progression. Advanced glycation end products (AGEs) and the renin-angiotensin system (RAS) play key roles in hyperglycemic-induced glomerular hypertrophy. Glomerular hyperfiltration, mediated by the renin-angiotensin-aldosterone system (RAAS), impaired tubuloglomerular feedback, and increased capillary filtration coefficient, further contributes to increased glomerular filtration rate. Inflammation and oxidative stress, triggered by hyperglycemia and AGEs, promote kidney damage. Abnormal ECM accumulation, driven by hyperglycemia and the transforming growth factor-beta pathway, leads to structural changes. Hyperglycemia-induced microalbuminuria and proteinuria reflect early signs of kidney damage. Managing diabetic nephropathy poses challenges, but ongoing research offers potential solutions. Novel therapeutic targets, combination therapies, personalized medicine approaches, regenerative medicine, and gene therapy are being explored. Advancements in diagnostics, including targeted therapies and non-invasive tools, show promise in preventing or mitigating the progression of diabetic nephropathy. Understanding these mechanisms is crucial for early detection, glycemic control, blood pressure management, and targeted therapies to slow disease progression. Collaboration among healthcare stakeholders is essential in finding effective solutions for this complex condition. This review therefore highlights the importance of a comprehensive approach to managing diabetic nephropathy and improving patient outcomes.
