Key result
Non-valvular atrial fibrillation was associated with a marked increase in leukocyte ROCK1 and ROCK2 gene expressions compared to healthy controls (P<0.0001).
Why the study?
Data were limited regarding the contribution of the Rho/Rho-kinase (ROCK) pathway to atrial fibrillation development.
Are leukocyte RHO/ROCK gene expressions altered in patients with non-valvular atrial fibrillation compared to matched controls?
Case-Control (n=84)
No
Are leukocyte RHO/ROCK gene expressions altered in patients with non-valvular atrial fibrillation compared to matched controls?
Leukocyte RHO/ROCK gene expressions are significantly altered in patients with non-valvular atrial fibrillation, suggesting a potential role in its pathogenesis via inflammatory cascades.
Leukocyte RHO/ROCK expression in NVAF is hypothesis-generating; larger prospective studies needed before any clinical consideration.
Atrial fibrillation (AF) is an arrhythmia caused by disorganized electrical activity in the atria, and it is an important cause of mortality and morbidity. There is a limited data about Rho/Rho‑kinase (ROCK) pathway contribute to AF development. The aim of the present study was to elucidate leukocyte RHO/ROCK gene expressions in patients with non‑valvular AF (NVAF). A total of 37 NVAF patients and 47 age and sex‑matched controls were included in this study. mRNA was extracted from leukocytes, and real‑time polymerase chain reaction was used for gene expression analysis. A marked increase in ROCK1 and ROCK2 gene expressions in patients with NVAF was observed (P<0.0001). The present study detected significant elevations in RHOBTB2, RND3 (RHOE), RHOC, RHOG, RHOH, RAC3, RHOB, RHOD, RHOV, RHOBTB1, RND2, RND1 and RHOJ gene expressions (P<0.01). However, there were marked decreases in CDC42, RAC2, and RHOQ gene expressions in patients with NVAF. No significant modifications were seen in the other Rho GTPase proteins RHOA, RAC1, RHOF, RHOU and RHOBTB3. To the best of our knowledge, the present study is the first to provide data that gene expression of leukocyte RHO/ROCK may contribute to the NVAF pathogenesis through activated leukocytes, which promotes the immune or inflammatory cascade.
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D�zen et al. (2019) conducted a case-control in Non-valvular atrial fibrillation (n=84). Non-valvular atrial fibrillation vs. Healthy controls was evaluated on Leukocyte ROCK1 and ROCK2 gene expressions (p=<0.0001). Non-valvular atrial fibrillation was associated with a marked increase in leukocyte ROCK1 and ROCK2 gene expressions compared to healthy controls (P<0.0001).
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