ArticleCurrent medicinal chemistry2026
A Genetic Perspective to Reveal the Impact of Mitochondrial Dysfunction-related Genes on Diabetic Kidney Disease: A Multi-omics Study.
Article in Current medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Renal proteomics of male offspring exposed to maternal protein restriction: molecular, epigenetic, and nephron-specific signatures of metabolic programming.Journal of physiology and biochemistry · 2026Article
- New Insights into the Role of Mitochondrial Dysfunction in Diabetic Kidney Disease in the Omics Era.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
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Authors and funding
5 authors.
Funding
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Abstract
objectiveThis study investigated the causes of Mitochondrial Dysfunction (MD) in Diabetic Kidney Disease (DKD) progression, and identified genes associated with DKD, especially those with significant genetic causal effects, to provide a theoretical basis for DKD treatment.
methodsUsing a large database and single-cell RNA sequencing (scRNA-seq) data, 333 MDRDEGs were discovered. MDRDEGs were linked to AGE-RAGE signaling, RNA processing, protein transport, and energy metabolism using functional enrichment analysis. Seven MDRDEGs with significant genetic causal effects in DKD were discovered using SMR and MR analyses: ACTN1, ALG11, CCNB1, HIVEP2, MANBA, TUBA1A, and WFS1. Co-localization and scRNA-seq analyses examined these genes' DKD connections. Due to the high significance of its prediction model and DKD expression, ACTN1 was studied in depth. PheWAS and molecular dynamics analysis assessed ACTN1's safety and efficacy as a therapeutic target, and its connection with other symptoms. ACTN1 protein expression in DKD tissues was confirmed by immunofluorescence.
resultsFunctional enrichment analysis revealed that MDRDEGs were mostly related to AGE-RAGE signaling, RNA processing, protein transport, and energy metabolism. Seven MDRDEGs caused DKD genetically in SMR and MR investigations. Genetic variations in ACTN1, ALG11, MANBA, and TUBA1A were linked to DKD by co-localization studies. scRNA-seq showed a dramatic increase in ACTN1 expression in DKD. Molecular dynamics analysis demonstrated that Dihydroergocristine can safely bind to ACTN1, while the PheWAS investigation found no significant relationships. DKD tissues exhibited higher ACTN1 protein levels via immunofluorescence. DISCUSSION: This study identified MDRDEGs linked to inflammation, cytoskeletal stabilization, and glucose metabolism pathways critical in Diabetic Kidney Disease (DKD) pathogenesis, highlighting their clinical potential as therapeutic targets. Notably, ACTN1 emerged as a causally linked gene overexpressed in DKD, with the prediction of dihydroergocristine as a targeting compound, offering novel avenues for clinical intervention.
conclusionThis study suggests that ACTN1 may be a therapeutic target for DKD and sheds light on its molecular pathogenesis, clinical prevention, and treatment.
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