Abraham Ehinomhen Ubhenin1 
,
Joshua Onyeka Ikebuiro2,
Fatima Anura1,
Ramatu Iya Idris1,
Osayemwenre Erharuyi3
For correspondence:- Abraham Ubhenin Email: ehibram@yahoo.co.uk Tel:+2348133893080
Accepted: 25 November 2023 Published: 31 December 2023
Citation: Ubhenin AE, Ikebuiro JO, Anura F, Idris RI, Erharuyi O. Novel approaches and therapeutic targets for diabetic nephropathy: Advances and promising strategies. Trop J Pharm Res 2023; 22(12):2567-2574 doi: 10.4314/tjpr.v22i12.21
© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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.
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