What question did this study set out to answer?

This research aims to explore how alogliptin affects diabetic cardiomyopathy (DCM) and its signaling mechanisms.

January 10, 2026The Kaohsiung Journal of Medical Sciences0 citationsOpen Access

Alogliptin Reduces Oxidative Stress in Cardiomyocytes and Ameliorates Diabetic Cardiomyopathy via the AURKB / NLGN2 Signaling

Q: What does this research mean for the field?

Alogliptin reduces oxidative stress and improves cardiomyocyte viability in diabetic cardiomyopathy mice by upregulating AURKB and activating NLGN2. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

LJLi‐Jing JiaoHebei Medical University JZJ W ZhouHebei Medical University JWJing WangHebei Medical University

Key Result

Alogliptin reduced oxidative stress and improved cardiomyocyte viability in diabetic cardiomyopathy mice by upregulating AURKB and activating NLGN2.

Key Points

This research aims to explore how alogliptin affects diabetic cardiomyopathy (DCM) and its signaling mechanisms.
Constructed a DCM mouse model and treated it with alogliptin.
Used bioinformatics analysis to identify downstream targets affected by alogliptin.
Performed echocardiography to assess heart function parameters.
Evaluated myocardial damage and cardiomyocyte viability through cardiac histological staining.
Alogliptin significantly improved DCM in mice by reducing oxidative stress.
Downstream analysis revealed AURKB as a target of alogliptin, which activated NLGN2.
High glucose conditions showed increased apoptosis and reduced viability in cardiomyocytes, alleviated by alogliptin.

Structured PICO

Does alogliptin ameliorate diabetic cardiomyopathy and reduce oxidative stress in preclinical models?

Population

Streptozotocin-induced diabetic cardiomyopathy (DCM) mouse model and in vitro mouse cardiomyocytes treated with high glucose

Intervention

Alogliptin

Comparator

Untreated DCM mice and untreated high-glucose cardiomyocytes

Outcome

Heart function parameters, myocardial damage, collagenous fibrosis, and apoptosis of cardiomyocytessurrogate

Alogliptin ameliorates diabetic cardiomyopathy and oxidative stress in preclinical models by promoting AURKB expression to transcriptionally activate NLGN2.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

ABSTRACT Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus. This study investigated the effects of alogliptin on DCM and its underlying mechanisms. A DCM model was constructed and treated with alogliptin. Downstream targets of alogliptin were screened using bioinformatics analysis. An in vitro DCM model was constructed using mouse cardiomyocytes with a high concentration of glucose. Echocardiography was performed to measure the heart function parameters. Myocardial damage, collagenous fibrosis, and apoptosis of cardiomyocytes in mouse heart tissues were assessed using cardiac histological staining. AURKB and NLGN2 levels, ROS levels, MDA levels, SOD activity, and cardiomyocyte viability were determined. Alogliptin ameliorated DCM in mice. Bioinformatics analysis revealed that the target of alogliptin was AURKB, and the downstream target of AURKB was NLGN2. AURKB and NLGN2 levels were reduced in the heart tissues of streptozotocin‐induced mice. Combined knockdown of AURKB and NLGN2 inhibited the therapeutic effect of alogliptin in DCM mice. Alogliptin attenuated oxidative stress, increased viability, and decreased apoptosis in cardiomyocytes treated with high glucose, which were reversed by combined knockdown of AURKB and NLGN2. Overall, alogliptin ameliorated oxidative stress in cardiomyocytes and DCM in mice by promoting AURKB expression to transcriptionally activate NLGN2.

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