Dear Colleagues,

Kidney disease remains a global public health concern because of high morbidity and mortality, and significant healthcare costs are associated with this disease. Diabetes and hypertension are the major causes of chronic kidney disease, which gradually leads to reduced quality of life and well-being. Ischemia, hypoxia, exposure to nephrotoxic compounds, and infections are the leading causes of acute kidney injury, which is encountered in a variety of clinical settings and is characterized by a rapid decline in kidney function and the failure to regulate fluid, electrolyte, and acid–base balance. The kidney has a remarkable ability to repair and regenerate its morphology and functions. However, inflammatory response and incomplete or maladaptive repair of the kidney after acute injury can lead to fibrosis and chronic kidney disease. Thus, acute kidney injury is a major risk factor for chronic and end-stage renal diseases. The therapeutic strategies used to treat acute kidney injury are still insufficient and dialysis remains the major therapeutic intervention to improve kidney recovery and patient survival.

Acute injury and chronic disease of the kidney in humans are multifactorial events. The pathogenesis of acute kidney injury is associated with a series of cellular responses to the initial insult that involve different cellular compartments, pathways and mechanisms, and a large variety of molecular targets. These responses involve protein unfolding and loss of function, DNA damage, cell cycle and growth arrest, mitochondrial dysfunction and changes in the energy metabolism, endoplasmic reticulum and oxidative stress, alterations in gene transcription and translation, disruption of biosignaling pathways, innate immune response, increased autophagy, and cell death. If the injury and stress are not too severe, repair processes are activated to replace lost cells, restore cellular metabolism and functions, and recover kidney functions. If the insult is prolonged or too severe, cellular stress and tissue dysfunction continue and the inflammatory cells are recruited to the kidney, initiating a sequelae of events leading to inflammation, fibrosis, and eventually the progressive loss of function characteristic of chronic kidney disease. Progress made in understanding these complex pathophysiological mechanisms and cellular events resulted in the development of several new biomarkers to diagnose acute kidney injury and its progression to chronic kidney disease. Hopefully, the continuation of studies into these areas will lead to the development of therapeutic approaches that prevent and/or treat acute kidney injury, or block the progression to chronic and end-stage renal diseases.

This Special Issue of IJMS seeks manuscripts that 1) identify subcellular and molecular targets that are involved in mediating renal cell injury, preventing injury of renal cells, and/or promoting repair of these cells after injury, 2) elucidate cellular, subcellular, and molecular mechanisms and pathways mediating kidney injury, repair, and recovery, 3) describe new animal models that better represent these mechanisms in human kidneys, and 4) propose therapeutic interventions to diminish or treat kidney injury or promote kidney recovery. We encourage scientists working in this area of research to submit original research articles, communications, or critical reviews that synthesize the current literature and discuss emerging directions. Thus, these studies will contribute to the development of therapeutic interventions that target the mechanisms of kidney injury and repair.

Prof. Dr. Grazyna Nowak
Guest Editor

• Pathogenesis of acute and chronic kidney injury
• Ischemic and nephrotoxic kidney injury
• Glomerular/interstitial/vascular damage
• Tubular necrosis, necroptosis, apoptosis, pyroptosis, and ferroptosis
• Inflammatory signals and fibrosis
• Bioenergetics, mitochondrial damage and biogenesis
• Autophagy and mitophagy
• Transcription factors in kidney injury
• Receptors and signaling pathways
• Cell cycle proteins
• Biomarkers
• Renal repair and regeneration
• Cytoprotection and therapeutic intervention
• In vivo and in vitro models of kidney injury