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吡非尼酮可增加梗死大鼠心肌中的横小管长度。

Pirfenidone increases transverse tubule length in the infarcted rat myocardium.

作者信息

Moammer Hussam, Bai Jizhong, Jones Timothy L M, Ward Marie, Barrett Caroyln, Crossman David J

机构信息

Manaaki Manawa-The Centre for Heart Research, Department of Physiology, School of Medical and Health Sciences, Faculty of Medical and Health Sciences, Waipapa Taumata Rau / The University of Auckland, Park Road, Grafton, Auckland, New Zealand.

Department of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.

出版信息

Interface Focus. 2023 Dec 15;13(6):20230047. doi: 10.1098/rsfs.2023.0047. eCollection 2023 Dec 6.

Abstract

Transverse (t)-tubule remodelling is a prominent feature of heart failure with reduced ejection fraction (HFrEF). In our previous research, we identified an increased amount of collagen within the t-tubules of HFrEF patients, suggesting fibrosis could contribute to the remodelling of t-tubules. In this research, we tested this hypothesis in a rodent model of myocardial infarction induced heart failure that was treated with the anti-fibrotic pirfenidone. Confocal microscopy demonstrated loss of t-tubules within the border zone region of the infarct. This was documented as a reduction in t-tubule frequency, area, length, and transverse elements. Eight weeks of pirfenidone treatment was able to significantly increase the area and length of the t-tubules within the border zone. Echocardiography showed no improvement with pirfenidone treatment. Surprisingly, pirfenidone significantly increased the thickness of the t-tubules in the remote left ventricle of heart failure animals. Dilation of t-tubules is a common feature in heart failure suggesting this may negatively impact function but there was no functional loss associated with pirfenidone treatment. However, due to the relatively short duration of treatment compared to that used clinically, the impact of long-term treatment on t-tubule structure should be investigated in future studies.

摘要

横管(T管)重塑是射血分数降低的心力衰竭(HFrEF)的一个显著特征。在我们之前的研究中,我们发现HFrEF患者的T管内胶原蛋白含量增加,提示纤维化可能导致T管重塑。在本研究中,我们在心肌梗死诱导的心力衰竭啮齿动物模型中验证了这一假设,该模型用抗纤维化药物吡非尼酮进行治疗。共聚焦显微镜显示梗死边缘区T管缺失。这表现为T管频率、面积、长度和横向元件减少。吡非尼酮治疗8周能够显著增加边缘区内T管的面积和长度。超声心动图显示吡非尼酮治疗后无改善。令人惊讶的是,吡非尼酮显著增加了心力衰竭动物左心室远隔部位T管的厚度。T管扩张是心力衰竭的一个常见特征,提示这可能对功能产生负面影响,但吡非尼酮治疗未导致功能丧失。然而,由于与临床使用的治疗时间相比,本研究治疗时间相对较短,未来研究应探讨长期治疗对T管结构的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5f9/10722216/2e8e2c0a4d80/rsfs20230047f01.jpg

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