Table 2.

Pathogenetic factors which can impair podocyte function in aging-related glomerulosclerosis and probably protective drugs-intervention

Mechanism/site		Podocyte lesion	Expected renal dysfunction	Probably protecting drug or intervention
Increased sympathetic adrenergic activity	Adrenergic receptor activation	Podocyte constriction	Decreased glomerular permeselectivity	Sympathicolytic agent
Increased intrarenal Ang II activity	Increase in free cytosolic calcium	Podocyte depolarization	Proteinuria	Inhibitor TRPC6
Desreased NO bioavailability	Deranged actin cytoskeleton by GTPase dynamin	effacement	Proteinuria	Nitric oxide donors ADMA inhibitors
Increased ET-1 availability	Distruption actin cytoskeleton. Dysfunction slit diaphragm	Sclerosis effacement detachment	Renal failure proteinuria	Endothelin antagonists
Increased oxidative stress (ROS)	ROS as second messanger for several transcription factors such as nuclear factor kB. Telomerase shortnes	Apoptosis detachment hyperthrophy	Proteinuria sclerosis	Antioxidant
Telomeres shortening	Decreased telomerase activity	Impaired podocyte repair (senescence)	Proteinuria	Telomerase activity reactivation