Correction to “Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy”

IF 2.8 4区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Cardiovascular Therapeutics Pub Date : 2026-07-13 DOI:10.1155/cdr/9810149

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引用次数: 0

Abstract

X. Wang, X. Zhang, H. Tang, et al., “Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy,” Cardiovascular Therapeutics 2026 (2026): 8401037, https://doi.org/10.1155/cdr/8401037

In this above article, there was an error in the affiliation. The correct affiliation list and author affiliations are shown below.

Xiangkun Wang¹, Xiaoyu Zhang², Huaiguang Tang¹, Xiaojuan Su³, Shutong Ding³, Xuelian Li⁴, and Bingong Li⁵

¹Department of Cardiology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China

²Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang Province, China

³School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, China

⁴Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

⁵Department of Cardiology, Qingdao Hospital of Rehabilitation University, East Hospital of Qingdao Municipal Hospital, Qingdao, Shandong, China

We apologize for this error.

查看原文本刊更多论文

更正“Asprosin通过促进线粒体自噬来保护缺氧/再氧化后的H9C2细胞免于铁凋亡”

王晓霞，张晓霞，唐宏，等，“Asprosin通过促进线粒体自噬保护H9C2细胞缺氧/再氧化后不发生铁凋亡”，《心血管治疗》2026 (2026):8401037,https://doi.org/10.1155/cdr/8401037In上述文章，归属错误。正确的隶属关系列表和作者隶属关系如下所示。王祥坤1，张晓宇2，唐怀光1，苏晓娟3，丁淑彤3，李雪莲4，李炳功1中国青岛大学青岛市市立医院心内科2中国黑龙江哈尔滨市哈尔滨医科大学第二附属医院神经内科3山东第二医科大学临床医学院，山东潍坊4同济医学院协和医院心内科，中国青岛华中科技大学，中国武汉5青岛康复大学附属医院心内科，青岛市市立医院东医院，中国山东省青岛市我们为这个错误道歉。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cardiovascular Therapeutics 医学-心血管系统

CiteScore

5.60

自引率

0.00%

发文量

审稿时长

6 months

期刊介绍： Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged. Subject areas include (but are by no means limited to): Acute coronary syndrome Arrhythmias Atherosclerosis Basic cardiac electrophysiology Cardiac catheterization Cardiac remodeling Coagulation and thrombosis Diabetic cardiovascular disease Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF) Hyperlipidemia Hypertension Ischemic heart disease Vascular biology Ventricular assist devices Molecular cardio-biology Myocardial regeneration Lipoprotein metabolism Radial artery access Percutaneous coronary intervention Transcatheter aortic and mitral valve replacement.