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Peer-reviewedCC BY 4.0Frontiers in Cell and Developmental Biology

Decreased expression of Acsm2 disrupts energy metabolism and affects cell death in acute kidney injury

  • Binyu Wang1,2
  • Yan Zha1,2
  1. 1Medical College, Guizhou University, GuiYang, China
  2. 2Department of Nephrology, Guizhou Provincial People’s Hospital, Guiyang, China
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Abstract

Background: Acute kidney injury (AKI) is a clinical syndrome characterized by high morbidity and a significant risk of mortality. Early diagnosis of AKI provides a crucial therapeutic window for treatment. There is an urgent need for universal biomarkers for the early diagnosis of AKI.

Methods: We analyzed single-cell RNA sequencing (scRNA-seq) data of AKI and found that Acsm2 was downregulated in the S1, S2, and S3 segments in AKI. Differential analysis, enrichment analysis, and pseudotime trajectory analysis were performed, in conjunction with animal experiments and transcriptome datasets, to explore the expression pattern and role of Acsm2 in AKI.

Results: Our study found that Acsm2 was significantly downregulated in the S1, S2, and S3 segments of renal tubules during the early stages of AKI. Acsm2 expression was correlated with key metabolic pathways, including fatty acid metabolism and mitochondrial function. The downregulation of Acsm2 in AKI was associated with disrupted energy metabolism and increased cell death, including apoptosis, necroptosis, and pyroptosis in proximal tubular cells (PTCs).

Conclusion: Downregulation of Acsm2 in AKI is correlated with impaired energy metabolism and cell death in PTCs, suggesting that Acsm2 may serve as a potential biomarker for the early diagnosis and intervention of AKI. Further studies on its mechanistic role could provide new insights into the pathophysiology of AKI and offer novel therapeutic strategies.

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Cite

BibTeXRIS
BibTeX
@article{wang2026decreased,
  title = {{Decreased expression of Acsm2 disrupts energy metabolism and affects cell death in acute kidney injury}},
  author = {Binyu Wang and Yan Zha},
  journal = {Frontiers in Cell and Developmental Biology},
  year = {2026},
  month = oct,
  doi = {10.3389/fcell.2026.1985288},
  url = {https://doi.org/10.3389/fcell.2026.1985288},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Decreased expression of Acsm2 disrupts energy metabolism and affects cell death in acute kidney injury
AU  - Binyu Wang
AU  - Yan Zha
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Cell and Developmental Biology
DO  - 10.3389/fcell.2026.1985288
UR  - https://doi.org/10.3389/fcell.2026.1985288
AB  - Background: Acute kidney injury (AKI) is a clinical syndrome characterized by high morbidity and a significant risk of mortality. Early diagnosis of AKI provides a crucial therapeutic window for treatment. There is an urgent need for universal biomarkers for the early diagnosis of AKI.  Methods: We analyzed single-cell RNA sequencing (scRNA-seq) data of AKI and found that Acsm2 was downregulated in the S1, S2, and S3 segments in AKI. Differential analysis, enrichment analysis, and pseudotime trajectory analysis were performed, in conjunction with animal experiments and transcriptome datasets, to explore the expression pattern and role of Acsm2 in AKI.  Results: Our study found that Acsm2 was significantly downregulated in the S1, S2, and S3 segments of renal tubules during the early stages of AKI. Acsm2 expression was correlated with key metabolic pathways, including fatty acid metabolism and mitochondrial function. The downregulation of Acsm2 in AKI was associated with disrupted energy metabolism and increased cell death, including apoptosis, necroptosis, and pyroptosis in proximal tubular cells (PTCs).  Conclusion: Downregulation of Acsm2 in AKI is correlated with impaired energy metabolism and cell death in PTCs, suggesting that Acsm2 may serve as a potential biomarker for the early diagnosis and intervention of AKI. Further studies on its mechanistic role could provide new insights into the pathophysiology of AKI and offer novel therapeutic strategies.
SN  - 2296-634X
ER  -