Key result
Endothelin-1 contributes to the progression of chronic kidney disease through blood pressure-independent mechanisms such as cell proliferation, podocyte dysfunction, inflammation, and fibrosis.
Why the study?
What is the role of endothelin-1 in renal disease, particularly its blood pressure-independent actions?
What is the role of endothelin-1 in renal disease, particularly its blood pressure-independent actions?
Endothelin-1 contributes to chronic kidney disease progression through blood pressure-independent mechanisms such as inflammation and fibrosis.
Answers are grounded in this paper and cite their sources.
ET antagonists may confer renoprotection beyond BP reduction in CKD; leaves open optimal targeting of BP-independent ET-1 effects.
Since its discovery over 20 years ago endothelin-1 (ET-1) has been implicated in a number of physiological and pathophysiological processes. Its role in the development and progression of chronic kidney disease (CKD) is well established and is an area of ongoing intense research. There are now available a number of ET receptor antagonists many of which have been used in trials with CKD patients and shown to reduce BP and proteinuria. However, ET-1 has a number of BP-independent effects. Importantly, and in relation to the kidney, ET-1 has clear roles to play in cell proliferation, podocyte dysfunction, inflammation and fibrosis, and arguably, these actions of ET-1 may be more significant in the progression of CKD than its prohypertensive actions. This review will focus on the potential role of ET-1 in renal disease with an emphasis on its BP-independent actions.
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Dhaun et al. (2012) conducted a review in Chronic kidney disease. Endothelin-1 was evaluated. Endothelin-1 contributes to the progression of chronic kidney disease through blood pressure-independent mechanisms such as cell proliferation, podocyte dysfunction, inflammation, and fibrosis.
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