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Aldehyde dehydrogenase-2 acts as a potential genetic target for renal fibrosis
Simin Tang1, Teng Huang2, Huan Jing3
1Department of Anesthesiology, The First People's Hospital of Foshan, Foshan, Guangdong Province, 528000, China; Sun Yet-Sen Memorial Hospital of Sun Yet-Sen University, Guangzhou, Guangdong Province, 510000, China.
Abstract:
Obstructive renal injury and drug-induced nephrotoxicity are the two most common causes of renal fibrosis diseases. However, whether these two different pathogeny induced same pathological outcomes contain common genetic targets or signaling pathway, the current research has not paid great attention. GSE121190 and GSE35257 were downloaded from the Gene Expression Omnibus (GEO) database. While GSE121190 represents a differential expression profile in kidney of mice with unilateral ureteral obstruction (UUO) model, GSE35257 represents cisplatin nephrotoxicity model. By using GEO2R, 965 differential expression genes (DEGs) in GSE121190 and 930 DEGs in GSE35257 were identified. 43 co-DEGs were shared and were extracted for protein-protein interaction (PPI) analysis. Subsequently, three shared pathways including glycolysis/gluconeogenesis, fatty acid degradation and pathways in cancer were involved in two models with Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. We reconfirmed that these three pathways have relatively high scores by using Gene Set Enrichment Analysis (GSEA) software. Additionally, further bioinformatic analysis showed that Aldehyde dehydrogenase-2 (Aldh2) involved in the progression of renal fibrosis by mediating glycolysis pathway. Then real-time PCR and western blotting were performed to validate the expression of Aldh2 in kidney tissue after three different etiologies that caused renal fibrosis. Basically consistent with our bioinformatics results, our experiment showed that the expression of Aldh2 is the most significantly decreased in the UUO model, followed by ischemia-reperfusion injury (IRI) model and finally the cisplatin-induced model. Thus, Aldh2 can act as a common potential genetic target for different renal fibrosis diseases.
Insights
Investigating common targets in renal fibrosis, this study identifies Aldehyde dehydrogenase-2 (Aldh2) as a potential genetic target. Aldh2 expression decreases across different kidney injury models, suggesting its role in fibrosis progression.
Area of Science:
- Nephrology
- Genomics
- Bioinformatics
Background:
- Renal fibrosis, a common outcome of obstructive nephropathy and drug-induced kidney injury, lacks fully understood common genetic targets.
- Previous research has not extensively explored shared molecular mechanisms between different causes of renal fibrosis.
Purpose of the Study:
- To identify common differential gene expression profiles and signaling pathways in distinct renal fibrosis models.
- To investigate Aldehyde dehydrogenase-2 (Aldh2) as a potential common therapeutic target for renal fibrosis.
Main Methods:
- Downloaded and analyzed gene expression datasets (GSE121190, GSE35257) from unilateral ureteral obstruction (UUO) and cisplatin nephrotoxicity models.
- Utilized GEO2R, protein-protein interaction (PPI) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) for bioinformatics analysis.
- Validated Aldh2 expression using real-time PCR and western blotting in kidney tissues from UUO, ischemia-reperfusion injury (IRI), and cisplatin-induced models.
Main Results:
- Identified 43 co-differential expression genes (co-DEGs) shared between UUO and cisplatin models.
- Discovered shared pathways including glycolysis/gluconeogenesis, fatty acid degradation, and pathways in cancer.
- Bioinformatic analysis highlighted Aldehyde dehydrogenase-2 (Aldh2) involvement in renal fibrosis via the glycolysis pathway.
- Experimental validation confirmed decreased Aldh2 expression in UUO, IRI, and cisplatin-induced renal fibrosis models, with the most significant decrease in the UUO model.
Conclusions:
- Aldehyde dehydrogenase-2 (Aldh2) plays a role in mediating renal fibrosis through the glycolysis pathway.
- Aldh2 exhibits decreased expression across various renal fibrosis etiologies, positioning it as a potential common genetic target for therapeutic intervention.
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