Abstract
Inflammation contributes a significant part to the advancement of diabetic kidney disease (DKD), yet relatively little is known about the root cause of these inflammatory events. Serum Amyloid A (SAA) triggers a potent inflammatory response in a variety of tissues and is up-regulated in glomerular and tubulointerstitial compartments of the diabetic kidney. Under inflammatory conditions, podocytes, along with other intrinsic cells, produce SAA locally in the kidney. Our recent work has shown that SAA induces NF-κB activation and subsequent inflammatory chemokines and cytokines in cultured podocytes. Recent evidence suggests that local production of SAA in diabetes may lead to monocyte and macrophage recruitment, neutrophil activation, and other related incidents resulting in sustained chronic inflammatory conditions in the kidney which may further exacerbate DKD.
Highlights
Diabetic kidney disease (DKD) is recognized as an inflammatory disease due to robust evidence that leukocytes are recruited to and cause injury in kidney tissue of patients with diabetic kidney disease (DKD) [1, 2]
Recent evidence suggests that local production of Serum Amyloid A (SAA) in diabetes may lead to monocyte and macrophage recruitment, neutrophil activation, and other related incidents resulting in sustained chronic inflammatory conditions in the kidney which may further exacerbate DKD
Our research has shown that advanced glycation end products (AGE) induce SAA up-regulation in glomerular podocytes through the advanced glycation end product receptor (RAGE) [8]
Summary
An inflammatory nexus: Serum amyloid A and inflammation in diabetic kidney disease. Inflammation contributes a significant part to the advancement of diabetic kidney disease (DKD), yet relatively little is known about the root cause of these inflammatory events. Serum Amyloid A (SAA) triggers a potent inflammatory response in a variety of tissues and is up-regulated in glomerular and tubulointerstitial compartments of the diabetic kidney. Podocytes, along with other intrinsic cells, produce SAA locally in the kidney. Our recent work has shown that SAA induces NF-κB activation and subsequent inflammatory chemokines and cytokines in cultured podocytes. Recent evidence suggests that local production of SAA in diabetes may lead to monocyte and macrophage recruitment, neutrophil activation, and other related incidents resulting in sustained chronic inflammatory conditions in the kidney which may further exacerbate DKD
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