Molecular Mechanisms of Kidney Injury

Dear Colleagues,

Renal disease is defined as a heterogeneous group of disorders affecting kidney structure and function. Acute kidney injury (AKI) is a complex syndrome that occurs in critically ill patients and has different etiologies such as sepsis, ischemia reperfusion (I/R) injury, nephrotoxin exposition or major surgery. Other factors, including diabetic status, hypertension, hypoxia, activation of the complement system, can lead to progression of chronic nephropathies. In recent years, research efforts have led to the hypothesis that each type of kidney injury, occurring in distinct kidney compartments (on endothelium, tubular, mesangial cells and podocytes, M1/M2 macrophages), preferentially activates pathway involved in inflammation, premature aging, CKD progression or cellular regeneration and survival. In addition, soluble factors released by damaged renal cells, extracellular vesicles or resident progenitor/stem cells could have an effect on the regulation of a pro-injury microenvironment. Deciphering the molecular mechanism of action underlying kidney injury and repair would provide early biomarkers to predict clinical outcome and targeted therapies to prevent the injury and delay the progression to chronic kidney disease. In this Special Issue, we will publish original research and reviews that would offer new insights into the molecular mechanisms of renal damage with a close scrutiny on factors acting as bifurcation point versus progression to CKD or kidney repair. 

Prof. Dr. Giuseppe Castellano
Dr. Rossana Franzin
Guest Editors

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