Advances in Understanding Molecular Mechanisms Involved in Chronic Kidney Injury and Repair
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 31 December 2024 | Viewed by 324
Special Issue Editor
Interests: kidney disease; obesity-related kidney disease; ischemic kidney injury; inflammation; oxidative stress; autophagy; ageing; extracellular vesicles; small ncRNA
Special Issue Information
Dear Colleagues,
The kidneys play a crucial role as excretory organs, preserving the internal environment of the organism. To maintain homeostasis, kidneys employ key physiological mechanisms, including glomerular filtration, tubular reabsorption, and tubular excretion. A decline in kidney function can give rise to a spectrum of health issues, including cardiovascular diseases, anemia, osteodystrophy, hyperlipidemia, and others. The renal proximal tubule serves as the primary sensor for different types of acute or chronic kidney insults, being particularly susceptible to cellular injury due to its essential functions in reabsorption, secretion, and substantial metabolic activity. Additionally, the renal tubule plays a pivotal role in the progression of both acute kidney injury (AKI) and chronic kidney disease (CKD). Depending on the severity of the kidney damage, initial injury can lead to regeneration of the damaged tissue or, in the case of sustained damage, the initiation of dramatic cellular and molecular rearrangements including cell cycle arrest, partial epithelial-mesenchymal transition, lipotoxicity, autophagy deregulation, oxidative stress, inflammatory response, senescence, and the death of renal tubular cells. As the process progresses, the renal parenchyma fails to regenerate and undergo maladaptive repair, promoting renal fibrosis and progress towards CKD, known as AKI-to-CKD transition. The precise cellular and molecular mechanisms behind kidney injury and repair remain incomplete. While the quest for effective therapies for chronic kidney injury persists, current options are limited to supportive therapy. Studies conducted in preclinical settings have identified various strategies that reduce fibrosis in experimental models, involving the targeting of signaling pathways, transcription factors, cytokines, or microRNAs.
As the guest editor of this Special Issue, “Advances in Understanding Molecular Mechanisms Involved in Chronic Kidney Injury and Repair”, in IJMS, I expect submissions from researchers focusing on deciphering molecular mechanisms of kidney injury and repair with a strong emphasis on molecular biology and molecular medicine. Original research papers and comprehensive up-to-date review articles are all welcome.
Dr. Milica Bozic
Guest Editor
Manuscript Submission Information
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Keywords
- kidney disease
- ischemic kidney injury
- renal fibrosis
- obesity
- inflammation
- oxidative stress
- autophagy
- senescence
- cell death
- small ncRNA
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