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Related Concept Videos

Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury II: Pathophysiology01:29

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...

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Updated: Jul 6, 2026

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
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Published on: May 15, 2021

ACSS2 Inhibition Alleviates Cisplatin-Induced Acute Kidney Injury: Insights from Targeted Metabolomics.

Wanting Chen1,2, Xian Zhao3, Jiaxin Zheng4

  • 1Affiliated Jiangning Chinese Medicine Hospital, China Pharmaceutical University, Nanjing 211100, P. R. China.

Chemical Research in Toxicology
|July 4, 2026
PubMed
Summary

Cisplatin chemotherapy causes kidney damage by disrupting fatty acid metabolism. Targeting the enzyme ACSS2 may protect against this cisplatin-induced acute kidney injury (AKI).

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Area of Science:

  • Biochemistry
  • Nephrology
  • Metabolomics

Background:

  • Cisplatin (DDP) is a vital chemotherapy drug, but its use is restricted by kidney toxicity.
  • Metabolic changes, particularly in fatty acid oxidation (FAO), are implicated in DDP-induced acute kidney injury (AKI), but specific enzymes involved are not fully understood.

Purpose of the Study:

  • To investigate the role of FAO-associated metabolic pathways and enzymes in DDP-induced AKI.
  • To identify potential therapeutic targets for mitigating DDP nephrotoxicity.

Main Methods:

  • Targeted metabolomic profiling of kidney tissue.
  • Analysis of acyl-CoA synthetase short-chain family member 2 (ACSS2) expression and function in cell and animal models of AKI.
  • In vivo pharmacological inhibition of ACSS2.

Main Results:

  • DDP treatment led to a significant blockade in FAO, indicated by altered fatty acid and acylcarnitine levels.
  • ACSS2 was identified as a key downregulated enzyme in DDP-induced AKI and also in ischemia/reperfusion AKI.
  • ACSS2 overexpression worsened DDP-induced kidney cell damage, while ACSS2 knockdown protected against it.
  • Inhibition of ACSS2 in vivo reduced DDP-induced AKI, oxidative stress, and improved kidney function.

Conclusions:

  • ACSS2 plays a critical role in the pathogenesis of DDP-induced AKI.
  • Targeting ACSS2 presents a potential therapeutic strategy to reduce cisplatin nephrotoxicity and improve kidney outcomes.