Article
Engineering, Biomedical
Wenqiang Qian, Daozhou Liu, Ying Han, Miao Liu, Bao Liu, Qifeng Ji, Bangle Zhang, Qibing Mei, Siyuan Zhou, Ying Cheng
Summary: Simultaneous inhibition of ferroptosis and apoptosis of cardiomyocytes can be a promising strategy to treat myocardial ischemia-reperfusion injury (MI/RI). Taking advantage of the highly expressed transferrin receptor in ischemic myocardium, cyclosporin A (CsA) was wrapped with apoferritin (ApoFn) to actively target and inhibit both ferroptosis and apoptosis in MI/RI mice, resulting in the restoration of cardiac function.
ACTA BIOMATERIALIA
(2023)
Article
Cardiac & Cardiovascular Systems
Fangying Yan, Rongchen Liu, Xinyu Zhuang, Ruoshui Li, Haiming Shi, Xiufang Gao
Summary: The study demonstrated that salidroside attenuates doxorubicin-induced cardiac dysfunction through activation of the QKI/FoxO1 pathway.
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
(2021)
Article
Neurosciences
Jing Tang, Yiang Chen, Jinyuan Li, Shuo Yan, Zenan Wang, Xinyu Deng, Ke Feng, Yanshuo Zhang, Chunrong Chen, Huixia Geng, Yanming Wang, Lai Wang
Summary: This study explores the neuroprotective effects of 14, 15-EET on mitochondrial dynamics after cerebral ischemia-reperfusion and its underlying mechanisms. The results demonstrate that 14, 15-EET can reduce neuronal apoptosis and cerebral infarction volume, protect neuronal structural integrity, and alleviate neurological impairment. Mechanistically, 14, 15-EET regulates mitochondrial division and fusion through the phosphorylation of AMPK and the upregulation of SIRT1, preserving mitochondrial dynamics and promoting neuroprotection.
CNS NEUROSCIENCE & THERAPEUTICS
(2023)
Article
Multidisciplinary Sciences
Rongchuan Yue, Mingming Lv, Meide Lan, Zaiyong Zheng, Xin Tan, Xuemei Zhao, Yulong Zhang, Jun Pu, Lei Xu, Houxiang Hu
Summary: Irisin protects cardiomyocytes from I/R injury by attenuating ER stress and ER stress-induced apoptosis. Pre-treatment with irisin significantly reduces cytochrome c release and caspase-3 activation caused by H/R, reducing apoptosis and increasing cell viability.
SCIENTIFIC REPORTS
(2022)
Review
Biochemistry & Molecular Biology
Xavier R. Chapa-Dubocq, Keishla M. Rodriguez-Graciani, Nelson Escobales, Sabzali Javadov
Summary: Mitochondria, known as the powerhouse of the cell, regulate various cellular processes including ion homeostasis, energy production, and cell death. The inner mitochondrial membrane (IMM) plays a critical role in controlling mitochondrial metabolism and function. The volume of the mitochondrial matrix, regulated by ion transport mechanisms, influences IMM remodeling and can affect mitochondrial respiration and cell survival. Despite extensive research, the mechanisms underlying changes in matrix volume and IMM remodeling in response to energy and oxidative stressors remain poorly understood. This review summarizes previous studies and discusses the interplay between matrix volume regulation and IMM remodeling.
Article
Medicine, Research & Experimental
Dengke Ou, Dan Ni, Rong Li, Xiaobo Jiang, Xiaoxiao Chen, Hongfei Li
Summary: The present study reveals that galectin-1 serves a protective role in myocardial ischemia-reperfusion injury by reducing inflammation and apoptosis levels in cardiomyocytes, ultimately improving cardiac function.
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Sehwan Jang, Xavier R. Chapa-Dubocq, Yulia Y. Tyurina, Claudette M. St Croix, Alexandr A. Kapralov, Vladimir A. Tyurin, Hulya Bayir, Valerian E. Kagan, Sabzali Javadov
Summary: Ferroptosis is a programmed iron-dependent cell death associated with lipid peroxidation, particularly phospholipids. Mitochondria play a crucial role in ferroptosis by being sensitive to ferroptotic stimuli and contributing to lipid peroxidation. The transport of reduced glutathione to mitochondria through DIC and OGC carrier proteins plays a key role in ferroptosis, and inhibiting these carriers can aggravate the process. Additionally, dihydrolipoic acid acts as an essential cofactor for mitochondrial enzymes and can attenuate ferroptosis by directly reducing peroxidized phospholipids.
Article
Immunology
Rui-Ze Niu, Lu-Qiao Wang, Wei Yang, Li-Zhong Sun, Jie Tao, Huang Sun, Song Mei, Wen-Jie Wang, Ke-Xiang Feng, Dian-Lun Qian, Xiang-Feng Bai
Summary: This study uncovered the crucial role of miR-582-5p in MIRI, as it promotes cardiomyocyte apoptosis by inhibiting Creb1. Targeting miR-582-5p and Creb1 could be potential therapeutic strategies for MIRI treatment.
IMMUNITY INFLAMMATION AND DISEASE
(2022)
Article
Oncology
Haiyan Zhou, Lili Mo, Niwen Huang, Changchao Zou, Chao Li, Muzhi Lin, Bei Zhang, Bo Wei, Ping Li, Xiaoyun Si, Jingjing Chen, Wei Li, Xingde Liu, Bailong Hu
Summary: This study investigated the effects of 3-iodothyronamine (T1AM) on myocardial ischemia reperfusion injury (MIRI) and its underlying molecular mechanisms. T1AM reduced body temperature, improved cardiac function, and decreased infarction size caused by MIRI. T1AM inhibited apoptosis and protected against MIRI through the Akt/FoxO1 signaling pathway.
ANNALS OF TRANSLATIONAL MEDICINE
(2022)
Article
Cell Biology
Yifeng Xu, Boqian Wang, Xiaoxiao Liu, Yunfei Deng, Yanqi Zhu, Feng Zhu, Yanyan Liang, Hongli Li
Summary: This study investigated the role and mechanism of PARP1 in MIRI, demonstrating that inhibition of PARP1 can protect cardiomyocytes from MIRI by regulating autophagy. Additionally, it was found that Sp1, a transcription factor of PARP1, plays a role in this process by binding to the target gene promoter of PARP1 during transcription. These findings suggest that targeting PARP1 has great therapeutic potential for MIRI in the future.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Aleksandra Stamenkovic, Kimberley A. O'Hara, David C. Nelson, Thane G. Maddaford, Andrea L. Edel, Graham Maddaford, Elena Dibrov, MohamadReza Aghanoori, Lorrie A. Kirshenbaum, Paul Fernyhough, Michel Aliani, Grant N. Pierce, Amir Ravandi
Summary: Oxidized phosphatidylcholines (OxPC) generated during reperfusion injury induce cardiomyocyte death through ferroptosis, which can be attenuated by neutralization of OxPC or with ferrostatin-1. Understanding this pathway may lead to novel strategies for preventing cell death during myocardial reperfusion injury.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2021)
Article
Medical Laboratory Technology
Shunv Cai, Yixing Liu, Yun Cheng, Junbo Yuan, Jun Fang
Summary: The study demonstrated that Dex has protective effects on H9c2 cardiomyocytes exposed to H/R treatment, leading to increased cell viability, inhibited inflammatory response, suppressed apoptosis, and alleviated ER stress and oxidative stress. Dex inhibited the intrinsic pathway of apoptosis and enhanced the activation of the JAK2/STAT3 signaling pathway in H/R-treated H9c2 cells. Overall, Dex shows promise as a therapeutic agent for myocardial I/R.
JOURNAL OF CLINICAL LABORATORY ANALYSIS
(2022)
Article
Chemistry, Medicinal
Suhaini Sudi, Yee-Zheng Chin, Nur Syafinaz Wasli, Siat-Yee Fong, Sadia Choudhury Shimmi, Siew-Eng How, Caroline Sunggip
Summary: This study aimed to elucidate the mechanism underlying the cardioprotective effect of carpaine in embryonic cardiomyocytes. The results showed that carpaine promoted cell proliferation and upregulated cell cycle marker proteins. Additionally, carpaine attenuated oxidative stress-induced damage by activating specific signaling pathways.
Article
Biotechnology & Applied Microbiology
Mao Yang, Ningning Xi, Meng Gao, Yanwei Yu
Summary: Sitagliptin has a protective effect against I/R injury in cardiomyocytes, potentially by regulating SIRT3 and autophagy.
Article
Medicine, Research & Experimental
Yingcun Liu, Yuqing Fu, Xin Xue, Gang Tang, Liangyi Si
Summary: This study revealed that BRD2 protects cardiomyocytes from hypoxia-reoxygenation damage by activating the Nrf2/HO-1 signaling pathway, providing potential therapeutic targets for minimizing myocardial ischemia-reperfusion (I/R) injury.
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2023)
Article
Cell & Tissue Engineering
Michael D. Lovelace, Ben J. Gu, Steven S. Eamegdool, Michael W. Weible, James S. Wiley, David G. Allen, Tailoi Chan-Ling
Article
Physiology
Yue-Kun Ju, Bon Hyang Lee, Sofie Trajanovska, Gouliang Hao, David G. Allen, Ming Lei, Mark B. Cannell
FRONTIERS IN PHYSIOLOGY
(2015)
Article
Physiology
Jie Liu, Li Xin, Victoria L. Benson, David G. Allen, Yue-Kun Ju
FRONTIERS IN PHYSIOLOGY
(2015)
Review
Physiology
David G. Allen, Nicholas P. Whitehead, Stanley C. Froehner
PHYSIOLOGICAL REVIEWS
(2016)
Editorial Material
Physiology
D. G. Allen
Review
Biochemistry & Molecular Biology
Hakan Westerblad, David G. Allen
ANTIOXIDANTS & REDOX SIGNALING
(2011)
Article
Cardiac & Cardiovascular Systems
Marion C. Mohl, Siiri E. Iismaa, Xiao-Hui Xiao, Oliver Friedrich, Soeren Wagner, Vesna Nikolova-Krstevski, Jianxin Wu, Ze-Yan Yu, Michael Feneley, Diane Fatkin, David G. Allen, Robert M. Graham
CARDIOVASCULAR RESEARCH
(2011)
Article
Cardiac & Cardiovascular Systems
Yue-Kun Ju, Jie Liu, Bon Hyang Lee, Donna Lai, Elizabeth A. Woodcock, Ming Lei, Mark B. Cannell, David G. Allen
CIRCULATION RESEARCH
(2011)
Article
Biochemistry & Molecular Biology
David G. Allen, Nicholas P. Whitehead
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
(2011)
Article
Physiology
D. G. Allen, E. Clugston, Y. Petersen, I. V. Roeder, B. Chapman, R. Rudolf
JOURNAL OF APPLIED PHYSIOLOGY
(2011)
Article
Physiology
Bao-Ting Zhang, Nicholas P. Whitehead, Othon L. Gervasio, Trent F. Reardon, Molly Vale, Diane Fatkin, Alexander Dietrich, Ella W. Yeung, David G. Allen
JOURNAL OF APPLIED PHYSIOLOGY
(2012)
Article
Cell Biology
Othon L. Gervasio, William D. Phillips, Louise Cole, David G. Allen
JOURNAL OF CELL SCIENCE
(2011)
Review
Cardiac & Cardiovascular Systems
Yue-Kun Ju, Elizabeth A. Woodcock, David G. Allen, Mark B. Cannell
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2012)
Review
Physiology
David G. Allen, Sofie Trajanovska
FRONTIERS IN PHYSIOLOGY
(2012)