Publications by authors named "Wellington Caio Silva"
Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular changes. Mitochondrial dysfunction and oxidative and nitrosative stress have been reported in the pathophysiology of CRS3.
View Article and Find Full Text PDFIn kidney disease (KD), several factors released into the bloodstream can induce a series of changes in the heart, leading to a wide variety of clinical situations called cardiorenal syndrome (CRS). Reactive oxygen species (ROS) play an important role in the signaling and progression of systemic inflammatory conditions, as observed in KD. The aim of the present study was to characterize the redox balance in renal ischemia/reperfusion-induced cardiac remodeling.
View Article and Find Full Text PDFCalcium/calmodulin-dependent protein kinases (CaMKs) are key regulators of calcium signaling in health and disease. CaMKII is the most abundant isoform in the heart; although classically described as a regulator of excitation-contraction coupling, recent studies show that it can also mediate inflammation in cardiovascular diseases (CVDs). Among CVDs, cardiorenal syndrome (CRS) represents a pressing issue to be addressed, considering the growing incidence of kidney diseases worldwide.
View Article and Find Full Text PDFBackground: Renal ischemia/reperfusion induces a systemic inflammatory response that is directly related to the development of cardiac hypertrophy due to cardiorenal syndrome type 3. Classic inflammatory pathways have been extensively investigated in cardiovascular diseases, including the participation of inflammasome in caspase-1-dependent IL-1β cleavage.
Objective: In this study, we aimed to understand how lack of caspase-1 would impact the hypertrophic and apoptotic response in the heart after renal ischemia/reperfusion.
Article Synopsis
- Cardiac arrhythmias can occur after kidney injury, particularly following renal ischemia-reperfusion (I/R), and this study investigates the role of the NLRP3 immune sensor in this process.
- Mice lacking NLRP3 or CASP1 did not show increased levels of IL-1β or the prolonged QJ intervals associated with arrhythmias seen in wild-type mice after renal I/R, suggesting a critical role of this pathway in cardiac electrical disturbances.
- The study also indicates that macrophages may play a role as sensors of tissue injury, and treatments targeting IL-1β could be a potential therapeutic strategy to mitigate cardiac issues following renal injury.