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2014 ; 14
(1
): 22-33
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Renal endothelial dysfunction in diabetic nephropathy
#MMPMID24720460
Cheng H
; Harris RC
Cardiovasc Hematol Disord Drug Targets
2014[]; 14
(1
): 22-33
PMID24720460
show ga
Endothelial dysfunction has been posited to play an important role in the
pathogenesis of diabetic nephropathy (DN). Due to the heterogeneity of
endothelial cells (ECs), it is difficult to generalize about endothelial
responses to diabetic stimuli. At present, there are limited techniques
fordirectly measuring EC function in vivo, so diagnosis of endothelial disorders
still largely depends on indirect assessment of mediators arising from EC injury.
In the kidney microcirculation, both afferent and efferent arteries, arterioles
and glomerular endothelial cells (GEnC) have all been implicated as targets of
diabetic injury. Both hyperglycemia per se, as well as the metabolic consequences
of glucose dysregulation, are thought to lead to endothelial cell dysfunction. In
this regard, endothelial nitric oxide synthase (eNOS) plays a central role in EC
dysfunction. Impaired eNOS activity can occur at numerous levels, including
enzyme uncoupling, post-translational modifications, internalization and
decreased expression. Reduced nitric oxide (NO) bioavailability exacerbates
oxidative stress, further promoting endothelial dysfunction and injury. The
injured ECs may then function as active signal transducers of metabolic,
hemodynamic and inflammatory factors that modify the function and morphology of
the vessel wall and interact with adjacent cells, which may activate a cascade of
inflammatory and proliferative and profibrotic responses in progressive DN. Both
pharmacological approaches and potential regenerative therapies hold promise for
restoration of impaired endothelial cells in diabetic nephropathy.
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