Diabetes mellitus (DM) is a growing worldwide epidemic
health problem. More than 350 million people
worldwide are affected by DM, and one in three U.S. adults could have DM in
2050, if the current trends continue. Diabetic nephropathy (DN) is one of the
most important DM complications, and it continues to rank as the leading cause
of end-stage renal disease (ESRD) in the U.S. Patients must undergo either
dialysis or a kidney transplantation once DN progress to ESRD, which produces a
huge economic burden for society.
There is a pressing need to develop novel therapeutics for
preventing or delaying the progression of DN. Progressive glomerulosclerosis
and renal interstitial fibrosis are two characteristic pathological changes in
the kidney in DN. Glomerular sclerosis has been at the center of attention for
nephrologists.
however, increasing evidence suggests the renal tubule is a
primary site of injury during DN progression, and a significant positive
correlation between development of interstitial fibrosis and subsequent loss of
renal function is seen in DN patients. Activation of the EGFR (Epidermal Growth
Factor Receptor) has been implicated in diabetic kidney injury, studies by us and others have found that
chronic EGFR activation in diabetic kidney is detrimental, and inhibition of
EGFR activation by pharmacologic or genetic strategies markedly preserved renal
function and slowed DN progression.
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