Background: Diabetic nephropathy (DN) is an important diabetic microvascular
complication, and it is becoming the leading cause of end-stage renal disease worldwide. Unfortunately,
there are no effective therapies to treat established DN. Therefore, new therapeutic
targets are urgently required. Accumulating studies indicate that mitochondrial dysfunction
is central to the pathogenesis of DN, and therapies targeted mitochondria might effectively
delay the progression of DN.
Method: A structured search of previously research literature about mitochondrial structure
and function, mitochondrial DNA, mitochondrial biogenesis, mitochondrial dynamics change,
mitophagy, mitochondrial ROS, mitochondrial apoptosis and therapies targeted mitochondria
has been performed in several databases.
Result: 176 papers were included in this review, the results from these papers indicated that
mitochondrial dysfunction is a pivotal issue for the development of DN,
such as elevated oxidative stress induced by disorders of the mitochondrial respiratory chain
complex and mitochondrial dynamic disorders, mutation of mitochondrial DNA, mitochondrial
abnormal biogenesis, mitochondrial excessive fission, mitochondrial ROS overproduction.
In addition, several therapeutic agents targeting the mitochondria (e.g mitochondrial
ROS modulators, mitochondrial fragmentation inhibitors and mitochondrial biogenesis activators)
have shown perfect therapeutic effect and security for DN.
Conclusion: The finding of this review has further confirmed the vital role of mitochondrial
dysfunction in the progression of DN, management strategies for recovering the normal mitochondrial
function will offer potential novel therapeutic targets for DN.