Collagen type V, interstitial fibrosis and the substrate for atrial fibrillation.
Collagen type V, interstitial fibrosis and the substrate for atrial fibrillation.
复制标题
V 型胶原蛋白、间质纤维化和心房颤动的基质。
DOI:
10.1016/j.ijcha.2024.101356
复制
发表时间:
2024
期刊:
影响因子:
--
通讯作者:
VanWagoner,DavidR
中科院分区:
文献类型:
--
作者:
VanWagoner,DavidR
AF [7]. While the associations are novel and plausible, the utility of efforts to routinely assess these targets remains unclear. Although collagen type V is easily detectable, it remains a relatively small fraction of the overall burden of collagen in the ECM. It may be of interest in future studies to assess the relative abundance collagen type V in the atria of patients with underlying valvular disease, and to evaluate the upstream regulators of collagen V. The conventional wisdom in this field suggests that fibrosis, once established, is difficult or impossible to reverse. The authors cite a mouse study in which the minor expression of collagen type V had an oversized impact on scar size following myocardial infarction. Loss of collagen V was associated with increased scar size in an integrin dependent manner [8]. This study suggests that efforts to decrease the abundance of collagen V in the atria are likely contraindicated.Overall, this well-written paper from Kostin and colleagues provides new insights into our understanding of the relative abundance and possible roles of collagen V in human atria. The confocal imaging is impressive. It will be of interest to determine if this protein represents a target for therapeutic intervention, or an ECM protein whose abundance is critical. It notable that some patients with advanced valvular heart disease (4+ mitral valve prolapse) have extreme dilatation of the left atrium, while dilatation is modest in others. The role of collagen type V in the dilatation process is unclear, as is the balance between increased interstitial fibrosis and overall atrial dimensions on AF progression.