Evidence map›Paper›PMID 41183881›Full record

ArticleExperimental animals2026

Intron polymorphism in Camk2d is associated with ventricular arrhythmias in normal adult Sprague-Dawley rats.

Rong Luo, Chunyun Zhao, Yi Wang, Yilin He, Chang Liu, Xiaoping Li, Xin Cao

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Article in Experimental animals, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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7 authors.

Rong LuoInstitute of Geriatric Cardiovascular Disease, Chengdu Medical College, No. 783, Xindu Avenue, Xindu District, Chengdu, Sichuan Province 610500, P.R. China.
Chunyun ZhaoSchool of Acupuncture-Moxibustion and Tuina, Chengdu University of Traditional Chinese Medicine, 1166 Liutai Avenue, Wenjiang District, Chengdu 611137, Sichuan Province, P.R. China.
Yi WangSchool of Acupuncture-Moxibustion and Tuina, Chengdu University of Traditional Chinese Medicine, 1166 Liutai Avenue, Wenjiang District, Chengdu 611137, Sichuan Province, P.R. China.
Yilin HeInstitute of Geriatric Cardiovascular Disease, Chengdu Medical College, No. 783, Xindu Avenue, Xindu District, Chengdu, Sichuan Province 610500, P.R. China.
Chang LiuInstitute of Geriatric Cardiovascular Disease, Chengdu Medical College, No. 783, Xindu Avenue, Xindu District, Chengdu, Sichuan Province 610500, P.R. China.
Xiaoping LiDepartment of Cardiology, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, No. 32, West Second Section, Yihuanlu, Qingyang District, Chengdu, Sichuan Province 610072, P.R. China.
Xin CaoSchool of Acupuncture-Moxibustion and Tuina, Chengdu University of Traditional Chinese Medicine, 1166 Liutai Avenue, Wenjiang District, Chengdu 611137, Sichuan Province, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium/calmodulin-dependent protein kinase II (CAMKII) is a critical regulator of cardiac electrophysiology. However, the role of the four bases deletion polymorphism in Camk2d which codes delta subunit of CAMKII, particularly those involving intron sequences, remains poorly understood. This study aimed to investigate the impact of Camk2d c.1044+125_128delGTTT missing polymorphism on cardiac morphology and arrhythmogenesis in normal adult Sprague-Dawley (SD) rats. A total of 85 SD rats were genotyped by Sanger sequencing, revealing a distribution of 25.9% wild-type (WT), 48.2% heterozygous, and 25.9% homozygous variants. Echocardiography, Hematoxylin-Eosin staining, Masson's trichrome staining and transmission electron microscopy indicated no significant differences in cardiac structure or baseline function among the three groups. In freely moving rats, premature atrial arrhythmias were detected in 2 of 9 WT rats, 1 of 9 heterozygous rats, and 1 of 9 homozygous rats. Premature ventricular contractions (PVCs) were observed in none of 9 WT or homozygous rats, 3 of 9 heterozygous rats, with one heterozygous rat exhibiting frequent PVCs. Electrical programmed stimulation revealed a higher incidence of inducible atrial fibrillation in homozygous rats compared to WT rats and a higher incidence of inducible ventricular tachycardia in heterozygous rats compared to WT rats. These findings suggest that deletion polymorphism in the intron sequences of Camk2d are unexpectedly common in normal SD rat populations and that such polymorphism predispose to ventricular arrhythmias without overt structural heart disease. Our study highlights the potential arrhythmogenic risk associated with non-coding DNA sequence alterations in Camk2d and underscores the importance of genetic screening in experimental animal models.

Indexed as

Arrhythmias, CardiacCalcium-Calmodulin-Dependent Protein Kinase Type 2IntronsPolymorphism, GeneticTachycardia, VentricularVentricular Premature ComplexesAnimalsMaleRatsRats, Sprague-DawleyCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2d protein, ratCamk2ddeletion polymorphismintronventricular arrhythmia

Identifiers

PMID41183881
PMCPMC13100694

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.