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Molecular and Biochemical Advances in Kidney Diseases and Genetics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 435

Special Issue Editor


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Guest Editor
Department of Pathological Physiology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia
Interests: animal models of kidney diseases; aging; trace elements; pathophysiology

Special Issue Information

Dear Colleagues,

Over 850 million people suffer from kidney disorders (KDs), which are a serious and expanding public health concern. They also operate as a "disease amplifier" for diabetes, heart disease, and infections, and put a tremendous financial burden on society. Acute kidney injury (AKI) affects approximately 10–15% of hospitalized patients and occurs in more than 50% of those admitted to intensive care units. Despite its frequent occurrence in clinical settings, AKI remains poorly understood from a pathophysiological standpoint. Chronic kidney disease (CKD) is a progressive pathological condition characterized by a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2 and/or at least one indicator of renal function impairment, lasting for at least three months. It is a serious condition, the prevalence and incidence of which have been growing at an extremely high rate in the last few decades. A complex interaction of biological mechanisms characterizes chronic kidney disease (CKD). The pathophysiology and consequences of chronic kidney disease are driven primarily by inflammation, elevated oxidative and metabolic stress, endothelial dysfunction, vascular calcification resulting from inadequate calcium and phosphate metabolism, and coagulation abnormalities.
Nevertheless, even with the increasing awareness of the causes of kidney diseases, we remain significantly distant from fully comprehending the various mechanisms that contribute to kidney disorders. The purpose of this Special Issue, "Molecular and Biochemical Advances in Kidney Diseases and Genetics," is to offer a venue for the presentation of research on pathophysiology, biochemistry, molecular biology, and any other topics on the disruption of molecular mechanisms in the development of kidney diseases. We welcome original research articles and review articles that summarize developments in this area.

Prof. Dr. Silvio R. De Luka
Guest Editor

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Keywords

  • pathophysiology
  • molecular mechanisms
  • biomarkers
  • in silico data analysis
  • image analysis
  • animal models

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Published Papers (1 paper)

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Review

30 pages, 5443 KB  
Review
Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition
by Rossana Franzin, Monica Campioni, Anna Storelli, Gabriele Ruggieri, Sabrina Molino, Giorgio Ladisa, Anna Gallone, Marco Fiorentino, Loreto Gesualdo and Paola Pontrelli
Int. J. Mol. Sci. 2026, 27(12), 5207; https://doi.org/10.3390/ijms27125207 - 9 Jun 2026
Viewed by 126
Abstract
The kidney is a highly specialized organ that maintains systemic homeostasis through tightly coordinated cellular and molecular mechanisms. Renal parenchymal cells regulate metabolic waste excretion, electrolyte and acid–base balance, and blood pressure control—functions that rely on the dynamic integration of intracellular organelles. Recent [...] Read more.
The kidney is a highly specialized organ that maintains systemic homeostasis through tightly coordinated cellular and molecular mechanisms. Renal parenchymal cells regulate metabolic waste excretion, electrolyte and acid–base balance, and blood pressure control—functions that rely on the dynamic integration of intracellular organelles. Recent advances in molecular and biochemical research have highlighted how inter-organelle communication is essential for preserving renal cell function and adaptive responses to stress. This review focuses on the molecular crosstalk among key organelles—including the nucleus, endoplasmic reticulum (ER), Golgi apparatus, mitochondria, lysosomes, and peroxisomes—primarily in tubular epithelial cells. We discuss how these interactions coordinate metabolic signaling, protein homeostasis, redox balance, and energy production and how their disruption contributes to maladaptive pathways during acute kidney injury (AKI), ultimately promoting chronic kidney disease (CKD) transition. Particular focus is placed on emerging pathways linking organelle dysfunction to inflammation, fibrosis, and metabolic reprogramming. Furthermore, we highlight recent advances in genetics and molecular therapeutics targeting organelle communication, including modulation of ER stress responses, mitochondrial biogenesis, and lysosomal function. Clinically approved agents, such as mTOR inhibitors, and experimental approaches—such as chemical chaperones and mitochondrial transplantation—demonstrate the potential to restore organelle homeostasis and mitigate renal injury. Overall, elucidating the molecular networks governing organelle crosstalk provides critical insights into kidney disease pathogenesis and identifies novel targets for therapeutic intervention in AKI-to-CKD transition. Full article
(This article belongs to the Special Issue Molecular and Biochemical Advances in Kidney Diseases and Genetics)
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