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Ferroptosis: A new insight for treatment of acute kidney injury
Shiyang Li1,2,3,4, Rui Wang1,2,3,4, Yixue Wang1,2,3,4
1Traditional Chinese Medicine Integrated Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Abstract:
Acute kidney injury (AKI), one of the most prevalent clinical diseases with a high incidence rate worldwide, is characterized by a rapid deterioration of renal function and further triggers the accumulation of metabolic waste and toxins, leading to complications and dysfunction of other organs. Multiple pathogenic factors, such as rhabdomyolysis, infection, nephrotoxic medications, and ischemia-reperfusion injury, contribute to the onset and progression of AKI. However, the detailed mechanism remains unclear. Ferroptosis, a recently identified mechanism of nonapoptotic cell death, is iron-dependent and caused by lipid peroxide accumulation in cells. A variety of studies have demonstrated that ferroptosis plays a significant role in AKI development, in contrast to other forms of cell death, such as apoptosis, necroptosis, and pyroptosis. In this review, we systemically summarized the definition, primary biochemical mechanisms, key regulators and associated pharmacological research progress of ferroptosis in AKI. We further discussed its therapeutic potential for the prevention of AKI, in the hope of providing a useful reference for further basic and clinical studies.
Insights
Ferroptosis, a cell death pathway involving iron and lipid peroxides, is a key factor in acute kidney injury (AKI). Understanding ferroptosis offers new therapeutic strategies for preventing kidney damage.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Acute kidney injury (AKI) is a widespread clinical condition with high global incidence.
- AKI involves rapid renal function decline, leading to metabolic waste buildup and multi-organ dysfunction.
- Pathogenic factors include rhabdomyolysis, infection, nephrotoxic drugs, and ischemia-reperfusion injury, but mechanisms are not fully understood.
Purpose of the Study:
- To review the definition and biochemical mechanisms of ferroptosis.
- To summarize key regulators and pharmacological advancements related to ferroptosis in AKI.
- To discuss the therapeutic potential of targeting ferroptosis for AKI prevention.
Main Methods:
- Systematic review of existing literature on ferroptosis and AKI.
- Analysis of biochemical pathways and regulatory mechanisms of ferroptosis.
- Evaluation of current and emerging pharmacological interventions.
Main Results:
- Ferroptosis, characterized by iron-dependent lipid peroxide accumulation, is a distinct cell death mechanism in AKI.
- Studies indicate ferroptosis plays a significant role in AKI pathogenesis, differentiating it from apoptosis, necroptosis, and pyroptosis.
- Key regulators and pharmacological targets for ferroptosis in AKI have been identified.
Conclusions:
- Ferroptosis is a critical mechanism in the development of acute kidney injury.
- Targeting ferroptosis presents promising therapeutic avenues for AKI prevention and treatment.
- Further research into ferroptosis mechanisms and therapies is warranted for clinical application.
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