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559 results on '"Yeh, Yung-Hsin"'

22. miR-181b targets semaphorin 3A to mediate TGF-[beta]-induced endothelial-mesenchymal transition related to atrial fibrillation

Author

Lai, Ying-Ju, Tsai, Feng-Chun, Chang, Gwo-Jyh, Chang, Shang-Hung, Huang, Chung-Chi, Chen, Wei-Jan, and Yeh, Yung-Hsin

Subjects
Vascular endothelium -- Physiological aspects -- Health aspects, Atrial fibrillation -- Development and progression, MicroRNA -- Physiological aspects -- Health aspects, Transforming growth factors -- Physiological aspects -- Health aspects, Semaphorins -- Genetic aspects -- Health aspects -- Physiological aspects, Health care industry
Abstract

Atrial fibrosis is an essential contributor to atrial fibrillation (AF). It remains unclear whether atrial endocardial endothelial cells (AEECs) that undergo endothelial-mesenchymal transition (EndMT) are among the sources of atrial fibroblasts. We studied human atria, TGF-[beta]-treated human AEECs, cardiac-specific TGF-[beta]-transgenic mice, and heart failure rabbits to identify the underlying mechanism of EndMT in atrial fibrosis. Using isolated AEECs, we found that miR-181b was induced in TGF-[beta]-treated AEECs, which decreased semaphorin 3A (Sema3A) and increased EndMT markers, and these effects could be reversed by a miR-181b antagomir. Experiments in which Sema3A was increased by a peptide or decreased by a siRNA in AEECs revealed a mechanistic link between Sema3A and LIM-kinase 1/phosphorylated cofilin (LIMK/p-cofilin) signaling and suggested that Sema3A is upstream of LIMK in regulating actin remodeling through p-cofilin. Administration of the miR181b antagomir or recombinant Sema3A to TGF-[beta]-transgenic mice evoked increased Sema3A, reduced EndMT markers, and significantly decreased atrial fibrosis and AF vulnerability. Our study provides a mechanistic link between the induction of EndMT by TGF-[beta] via miR-181b/Sema3A/LIMK/p-cofilin signaling to atrial fibrosis. Blocking miR-181b and increasing Sema3A are potential strategies for AF therapeutic intervention., Introduction Atrial fibrillation (AF) is the most common sustained arrhythmia and results in increased morbidity and mortality. Rhythm control in persistent long-term AF, which is characterized by severe atrial myocyte [...]

Published
2022
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30. Aldehyde Dehydrogenase 2 (ALDH2) Deficiency, Obesity, and Atrial Fibrillation Susceptibility: Unraveling the Connection.

Author

Hsu, Lung-An, Yeh, Yung-Hsin, Chang, Chi-Jen, Chen, Wei-Jan, Tsai, Hsin-Yi, and Chang, Gwo-Jyh

Subjects
*NUCLEAR factor E2 related factor, *ALDEHYDE dehydrogenase, *TRANSFORMING growth factors-beta, *EAST Asians
Abstract

Atrial fibrillation (AF), characterized by structural remodeling involving atrial myocardial degradation and fibrosis, is linked with obesity and transforming growth factor beta 1 (TGF-β1). Aldehyde dehydrogenase 2 (ALDH2) deficiency, highly prevalent in East Asian people, is paradoxically associated with a lower AF risk. This study investigated the impact of ALDH2 deficiency on diet-induced obesity and AF vulnerability in mice, exploring potential compensatory upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme-oxygenase 1 (HO-1). Wild-type (WT) and ALDH2*2 knock-in (KI) mice were administered a high-fat diet (HFD) for 16 weeks. Despite heightened levels of reactive oxygen species (ROS) post HFD, the ALDH2*2 KI mice did not exhibit a greater propensity for AF compared to the WT controls. The ALDH2*2 KI mice showed equivalent myofibril degradation in cardiomyocytes compared to WT after chronic HFD consumption, indicating suppressed ALDH2 production in the WT mice. Atrial fibrosis did not proportionally increase with TGF-β1 expression in ALDH2*2 KI mice, suggesting compensatory upregulation of the Nrf2 and HO-1 pathway, attenuating fibrosis. In summary, ALDH2 deficiency did not heighten AF susceptibility in obesity, highlighting Nrf2/HO-1 pathway activation as an adaptive mechanism. Despite limitations, these findings reveal a complex molecular interplay, providing insights into the paradoxical AF–ALDH2 relationship in the setting of obesity. [ABSTRACT FROM AUTHOR]

Published
2024
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32. Clinical Outcomes in Elderly Atrial Fibrillation Patients at Increased Bleeding Risk Treated with Very-Low-Dose versus Regular-Dose Non-Vitamin K Antagonist Oral Anticoagulants: a Nationwide Cohort Study

Author

Chan, Yi-Hsin, primary, Chao, Tze-Fan, additional, Chen, Shao-Wei, additional, Lee, Hsin-Fu, additional, Li, Pei-Ru, additional, Yeh, Yung-Hsin, additional, Kuo, Chi-Tai, additional, See, Lai-Chu, additional, and Lip, Gregory Y H, additional

Published
2023
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