Li, Shichao’s team published research in Cardiology in 2020 | 6823-69-4

Cardiology published new progress about Atrial fibrillation. 6823-69-4 belongs to class imidazoles-derivatives, and the molecular formula is C30H30Cl2N6O2, Name: p-Benzenediacrylanilide, 4′,4′′-di-2-imidazolin-2-yl-, dihydrochloride.

Li, Shichao; Gao, Yuanfeng; Liu, Ye; Li, Jing; Yang, Xiyan; Hu, Roumu; Liu, Jia; Zhang, Yuan; Zuo, Kun; Li, Kuibao; Yin, Xiandong; Chen, Mulei; Zhong, Jiuchang; Yang, Xinchun published the artcile< Myofibroblast-Derived Exosomes Contribute to Development of a Susceptible Substrate for Atrial Fibrillation>, Name: p-Benzenediacrylanilide, 4′,4′′-di-2-imidazolin-2-yl-, dihydrochloride, the main research area is atrial fibrillation myofibroblast cardiomyocyte exosome; Atrial fibrillation; Exosome; L-type calcium channel; Paracrine communication.

Atrial fibrosis plays a critical role in atrial fibrillation (AF). A key event in the pathogenesis of fibrosis is the activation of fibroblasts (FBs) into myofibroblasts (MFBs). Paracrine factors released from MFBs lead to ion channel expression changes in cardiomyocytes (CMs). Downregulation of L-type calcium channel Cav1.2 expression is a hallmark of AF-associated ionic remodeling. However, whether exosome-mediated crosstalk between MFBs and CMs regulates Cav1.2 expression remains unknown. Atrial FBs and CMs were isolated and cultured from neonatal rats by enzymic digestion. Untreated FBs expressed limited amounts of alpha smooth muscle actin (α-SMA), while angiotensin II induced a significant upregulation of α-SMA-expressing MFBs. Co-cultures of MFBs and CMs resulted in downregulation of Cav1.2 expression in CMs, which was largely abolished by pretreatment of MFBs with exosomal inhibitor GW4869. Addnl., the adrenergic receptor agonist-elicited Ca2 influx signals in CMs were remarkably attenuated by pretreatment with MFB-derived Exos, corresponding to the paralleled change in Cav1.2 expression. Finally, miR-21-3p, a potential Cav1.2-inhibitory miRNA, was enriched in MFB-derived Exos and upregulated in CMs in response to MFB-derived Exos. We uncover an Exo-mediated crosstalk between MFBs and CMs, contributing to increased vulnerability to AF by reducing the expression of Cav1.2 in CMs.

Cardiology published new progress about Atrial fibrillation. 6823-69-4 belongs to class imidazoles-derivatives, and the molecular formula is C30H30Cl2N6O2, Name: p-Benzenediacrylanilide, 4′,4′′-di-2-imidazolin-2-yl-, dihydrochloride.

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem