Sun, Wu, Lei, Luo, Zhang, Wang, Tang, Yang, Tian, Wang, Li, Zhang, Zhang, Li, & She (2026). SBK2-Driven NDUFV1 Phosphorylation and Translocation Limits Cardiac Hypertrophy.. Circulation research.
Sun, Wu, Lei, Luo, Zhang, Wang, et al. SBK2-Driven NDUFV1 Phosphorylation and Translocation Limits Cardiac Hypertrophy.. Circulation research. 2026; PMID: 42153297
Sun, Wu, Lei, et al. SBK2-Driven NDUFV1 Phosphorylation and Translocation Limits Cardiac Hypertrophy.[J]. Circulation research. 2026.
@article{sun2026,
author = {Sun and Wu and Lei and Luo and Zhang and Wang and Tang and Yang and Tian and Wang and Li and Zhang and Zhang and Li and She},
title = {SBK2-Driven NDUFV1 Phosphorylation and Translocation Limits Cardiac Hypertrophy.},
journal = {Circulation research},
year = {2026},
note = {PMID: 42153297},
}
TY - JOUR AU - Sun AU - Wu AU - Lei AU - Luo AU - Zhang AU - Wang AU - Tang AU - Yang AU - Tian AU - Wang AU - Li AU - Zhang AU - Zhang AU - Li AU - She TI - SBK2-Driven NDUFV1 Phosphorylation and Translocation Limits Cardiac Hypertrophy. T2 - Circulation research PY - 2026 AN - PMID:42153297 ER -
Heart failure remains a major global health burden, driven largely by pathological cardiac hypertrophy. Mitochondrial dysfunction, particularly impaired mitochondrial complex I activity, is central to the disease progression, yet its regulatory mechanisms are poorly understood. Cross-species transcriptomic screening and UK Biobank analyses identified SBK2 (Src homology 3 domain-binding kinase 2) as a conserved, cardiac-enriched kinase potentially linked to heart failure risk. We hypothesized that SBK2 regulates cardiac hypertrophy by modulating mitochondrial complex I function.