Rodent models to study type 1 and type 2 diabetes induced human diabetic nephropathy.

Abstract

Diabetic nephropathy (DN), an outcome of prolonged diabetes, has affected millions of people worldwide and every year the incidence and prevalence increase substantially. The symptoms may start with mild manifestations of the disease such as increased albuminuria, serum creatinine levels, thickening of glomerular basement membrane, expansion of mesangial matrix to severe pathological symptoms such as glomerular lesions and tubulointerstitial fibrosis which may further proceed to cardiovascular dysfunction or end-stage renal disease. Numerous therapeutic interventions are being explored for the management of DN, however, these interventions do not completely halt the progression of this disease and hence animal models are being explored to identify critical genetic and molecular parameters which could help in tackling the disease. Rodent models which mostly include mice and rats are commonly used experimental animals which provide a wide range of advantages in understanding the onset and progression of disease in humans and also their response to a wide range of interventions helps in the development of effective therapeutics. Rodent models of type 1 and type 2 diabetes induced DN have been developed utilizing different platforms and interventions during the last few decades some of which mimic various stages of diabetes ranging from early to later stages. However, a rodent model which replicates all the features of human DN is still lacking. This review tries to evaluate the rodent models that are currently available and understand their features and limitations which may help in further development of more robust models of human DN. Using these rodent models can help to understand different aspects of human DN although further research is required to develop more robust models utilizing diverse genetic platforms which may, in turn, assist in developing effective interventions to target the disease at different levels.