Abstract
One of the most frequent complications in patients with diabetes mellitus is diabetic nephropathy (DN). At present, it constitutes the first cause of end stage renal disease, and the main cause of cardiovascular morbidity and mortality in these patients. Therefore, it is clear that new strategies are required to delay the development and the progression of this pathology. This new approach should look beyond the control of traditional risk factors such as hyperglycemia and hypertension. Currently, inflammation has been recognized as one of the underlying processes involved in the development and progression of kidney disease in the diabetic population. Understanding the cascade of signals and mechanisms that trigger this maladaptive immune response, which eventually leads to the development of DN, is crucial. This knowledge will allow the identification of new targets and facilitate the design of innovative therapeutic strategies. In this review, we focus on the pathogenesis of proinflammatory molecules and mechanisms related to the development and progression of DN, and discuss the potential utility of new strategies based on agents that target inflammation.
Highlights
Diabetes has become a global health burden affecting 425 million people worldwide according to the International Diabetes Federation (IDF) [1]
We focus on the pathogenesis of the proinflammatory molecules and pathways related to the development and progression of diabetic nephropathy (DN), and discuss the opportunity of potential new strategies based on the agents that target the inflammation
colony-stimulating factor 1 (CSF1) is constitutively expressed in diverse renal cellular types, the disarrangement in the renal levels of this chemokine in chronic inflammation is involved in the progression of renal disease by generating an uncontrolled intrarenal amplification of macrophages
Summary
Diabetes has become a global health burden affecting 425 million people worldwide according to the International Diabetes Federation (IDF) [1]. Several therapeutic interventions have been implemented to slow the progression of DN These approaches have proved insufficient and new strategies are warranted. Both circulating inflammatory mediators and infiltration of immune cells levels into renal tissue have been found to be increased in animal models and in patients with DN [8,9,10,11,12,13,14,15,16,17,18]. The understanding of the inflammatory mechanisms involved in the development and progression of this disease will enable the identification of new potential targets and facilitate the design of innovative anti-inflammatory therapeutic strategies. We focus on the pathogenesis of the proinflammatory molecules and pathways related to the development and progression of DN, and discuss the opportunity of potential new strategies based on the agents that target the inflammation
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