Mechanisms of Kidney Injury and Treatment Modalities

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 993

Special Issue Editor


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Guest Editor
Health Sciences Centre, University of Louisville, Louisville, KY, USA
Interests: epigenetics; gaseous molecules; kidney disease; metabolic disorders; extracellular matrix; acute kidney injury; dysbiosis; hypertensive and diabetic nephropathy

Special Issue Information

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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Keywords

  • 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

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Published Papers (2 papers)

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Research

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18 pages, 7258 KiB  
Article
Integration of DNA Methylome and Transcriptome Analysis to Identify Novel Epigenetic Targets in the Acute Kidney Injury–Chronic Kidney Disease Transition
by Xumin Zheng, Xinru Guo, Yuhao Chen, Kaiting Zhuang, Na Gong, Yifei Fu, Yanjun Liang, Yue Xu, Siyang Wang, Wenjuan Wang, Xiangmei Chen and Guangyan Cai
Biomolecules 2025, 15(4), 498; https://doi.org/10.3390/biom15040498 - 29 Mar 2025
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Abstract
(1) Background: the epigenetic mechanisms underlying the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remain poorly understood; (2) Methods: to investigate this process, we conducted genome-wide DNA methylation sequencing to map the epigenetic changes during the AKI-CKD transition in [...] Read more.
(1) Background: the epigenetic mechanisms underlying the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remain poorly understood; (2) Methods: to investigate this process, we conducted genome-wide DNA methylation sequencing to map the epigenetic changes during the AKI-CKD transition in a mouse model. By integrating DNA methylome and transcriptome analyses, we identified genes and signaling pathways regulated by DNA methylation throughout this progression; (3) Results: our analysis identified four candidate genes—Atp1a3, Ncf1, Lpl, and Slc27a2—that were regulated by DNA methylation and strongly correlated with kidney disease prognosis. Additionally, we found that the PPAR signaling pathways, among others, were implicated in this process. Treatment with DNA methyltransferase inhibitors mitigated fibrosis and improved lipid metabolism in the kidneys during AKI-CKD progression; (4) Conclusions: this study provides the first comprehensive epigenetic map of the AKI-CKD transition. Our findings offer new insights into the epigenetic regulation of kidney disease progression and highlight potential therapeutic targets to prevent the transition from AKI to CKD. Full article
(This article belongs to the Special Issue Mechanisms of Kidney Injury and Treatment Modalities)
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Review

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23 pages, 1523 KiB  
Review
Mechanisms of Acute Kidney Injury–Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities
by Dongxue Xu, Xiaoyu Zhang, Jingjing Pang, Yiming Li and Zhiyong Peng
Biomolecules 2025, 15(6), 794; https://doi.org/10.3390/biom15060794 - 29 May 2025
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Abstract
Acute kidney injury (AKI) causes damage to the renal epithelium, initiating a reparative process intended to restore renal function. Although effective repair can result in the complete recovery of kidney function, this process is frequently incomplete. In instances where repair is unsuccessful, the [...] Read more.
Acute kidney injury (AKI) causes damage to the renal epithelium, initiating a reparative process intended to restore renal function. Although effective repair can result in the complete recovery of kidney function, this process is frequently incomplete. In instances where repair is unsuccessful, the kidney experiences maladaptive alterations that may progressively result in chronic kidney disease (CKD), a phenomenon referred to as failed repair. This condition is precipitated by hypotensive, septic, or toxic insults, which initiate a series of pathophysiological processes, including microcirculatory dysfunction, the activation of inflammatory responses, and the death of tubular epithelial cells. These events collectively compromise renal function and trigger a complex repair response. This review provides a comprehensive examination of the multifactorial mechanisms underlying the initiation and progression of AKI, the regenerative pathways facilitating structural recovery in severely damaged kidneys, and the critical transition from adaptive repair to maladaptive remodeling. Central to this transition are mechanisms such as epigenetic reprogramming, G2/M cell-cycle arrest, cellular senescence, mitochondrial dysfunction, metabolism reprogramming, and cell death, which collectively drive the progression of CKD. These mechanistic insights offer a robust foundation for the development of targeted therapeutic strategies aimed at enhancing adaptive renal repair. Full article
(This article belongs to the Special Issue Mechanisms of Kidney Injury and Treatment Modalities)
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