Role of Different Molecular Pathways in the Development of Diabetes-Induced NephropathyVirvikram Sharma* and Sharma PL
Department of Pharmacology, ISF College of Pharmacy, India
- *Corresponding Author:
- Virvikram Sharma
Department of Pharmacology
Isf College of Pharmacy b-1,665/19d
New Kundan Puri, Civil Lines, Ludhian
Indiana 141001, India
E-mail: [email protected]
Received date: February 05, 2013; Accepted date: April 28, 2013; Published date: May 04, 2013
Citation: Sharma V, Sharma PL (2013) Role of Different Molecular Pathways in the Development of Diabetes- Induced Nephropathy. J Diabetes Metab S9:004. doi:10.4172/2155-6156.S9-004
Copyright: © 2013 Sharma V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Diabetes mellitus is heterogeneous primary disorder of carbohydrate metabolism with multiple etiologic factors that generally involves absolute or relative insulin deficiency or insulin resistance or both, which results in hyperglycemia. According to WHO projection; it will be the single largest non-communicable disease worldwide by the year 2025 with the largest diabetic population in India. India leads the world with largest diabetic population thus, being termed the ‘‘Diabetes Capital of the World’’. However, the prevalence of diabetes is consistently increasing, but still an effective treatment is lacking for the management of this epidemic. The uncontrolled and chronic diabetes mellitus often leads to cardiomyopathy, macrovascular complications and microvascular complications that include retinopathy, neuropathy and nephropathy. Diabetic Nephropathy (DN) is mainly characterized by decreased Glomerular Filteration Rate (GFR), excessive deposition of extracellular matrix proteins, thickening of the peripheral glomerular basement membrane, glomerular hypertrophy, tubulointerstitial fibrosis, increased excretion of albumin and decreased creatinine clearance. Formation of Advanced Glycation End-Products (AGEs), activation of Protein Kinase C (PKC), c-Jun N-terminal kinase (JNK), Mitogen Activated Protein Kinases (MAPKs), oxidative stress are the possible molecular mechanisms of DN. Despite many molecular mechanisms, the pathophysiology of DN is not clearly understood and its management is unsatisfactory.