Mechanisms of Kidney Injury and Treatment Modalities

Dear Colleagues,

Kidney disease is a significant global public health concern due to its high rates of morbidity and mortality, as well as the substantial healthcare costs associated with it. The common causes of chronic kidney disease (CKD) are diabetes, hypertension, genetic disorder, infection, and drug toxicity, among others, which lead to the gradual deterioration of kidney health, quality of life, and overall well-being. Acute kidney injury (AKI) is characterized by a rapid decline in kidney function and the inability to regulate the fluid, electrolyte, and acid–base balance. Despite the kidney's ability to repair and regenerate its structure and functions, an inflammatory response or inadequate repair after acute injury can result in the development of CKD. This highlights that AKI is a significant risk factor for chronic and end-stage renal diseases. Currently, the therapeutic strategies available for treating AKI are inadequate, with dialysis being the primary intervention utilized to enhance kidney recovery and improve patient survival.

The development of AKI involves a series of cellular responses to the initial damage, including protein unfolding and loss of function, DNA damage, cell cycle and growth arrest, mitochondrial dysfunction, changes in energy metabolism, alteration of gene transcription, endoplasmic reticulum stress, altered immune response, cellular senescence, etc. Interestingly, if the injury and stress are not too severe, the body can activate repair processes to replace lost cells, restore cellular metabolism and functions, and recover kidney function. However, if the insult is prolonged or too severe, cellular stress and tissue dysfunction may persist, leading to the recruitment of inflammatory cells to the kidneys. This initiates a series of events that result in inflammation, fibrosis, and ultimately the progressive loss of function characteristic of CKD.

Recent advances in understanding these complex pathophysiological mechanisms and cellular events have led to the development of several new biomarkers for diagnosing AKI and monitoring its progression to CKD. Continued research in these areas holds promise for developing new and/or adjuvant therapeutic approaches to treat AKI and halt the progression to chronic and end-stage renal diseases.

This Special Issue of Biomolecules invites original research and review articles that focus on, but not limited to, the following areas: (1) elucidating the mechanisms and pathways involved in kidney injury and recovery; (2) identifying targets that prevent cellular injury or promote cell repair after injury; (3) studies on animal models and findings in human kidney diseases; and (4) comprehensive review articles on AKI/CKD.

Prof. Dr. Utpal Sen
Guest Editor

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• acute and chronic kidney injury
• autophagy and mitophagy
• bioenergetics, mitochondrial damage, and biogenesis
• current therapeutic modalities and future strategies
• epigenetic DNA methylation, histone modification, and non-coding RNAs and miRNAs
• gaseous molecules and signaling pathways
• gender differences, aging, and kidney dysfunction
• glomerulosclerosis and renovascular remodelling following injury
• gut–kidney axis and health
• hypertensive, diabetic, and IgA nephropathy
• inflammatory vs. reparatory macrophages and renal repair
• ischemia and reperfusion injury
• matrix protein, metalloproteinases, and their inhibitors
• necrosis, necroptosis, apoptosis, pyroptosis, and ferroptosis
• renal repair and regeneration