Article
Cardiac & Cardiovascular Systems
Hiran A. Prag, Dunja Aksentijevic, Andreas Dannhorn, Abigail Giles, John F. Mulvey, Olga Sauchanka, Luping Du, Georgina Bates, Johannes Reinhold, Duvaraka Kula-Alwar, Zhelong Xu, Luc Pellerin, Richard J. A. Goodwin, Michael P. Murphy, Thomas Krieg
Summary: Malonate selectively enters cardiomyocytes during reperfusion in a low pH environment caused by ischemia, protecting against cardiac ischemia/reperfusion injury.
CIRCULATION RESEARCH
(2022)
Review
Engineering, Biomedical
Tianjiao Zhao, Wei Wu, Lihua Sui, Qiong Huang, Yayun Nan, Jianhua Liu, Kelong Ai
Summary: This article discusses the biology and molecular mechanisms of myocardial ischemia reperfusion injury, and summarizes the application of ROS-based nanoparticles, highlighting the latest advances in nanotechnology research for the treatment of myocardial ischemia reperfusion injury.
BIOACTIVE MATERIALS
(2022)
Review
Biochemistry & Molecular Biology
Alessandro Parente, Mauricio Flores Carvalho, Andrea Schlegel
Summary: The endothelium, forming the inner layer of blood vessels, plays a crucial role in intercellular communication and vascular homeostasis. Recent studies have highlighted the importance of endothelial cells in metabolic function and their response to flow changes, which are linked to mitochondrial health. The impact of different perfusion conditions on liver sinusoidal endothelial cells (LSECs) and their mitochondrial function in the context of liver transplantation is discussed in this article. The available ex situ machine perfusion strategies and their effects on LSEC health are described, with a focus on specific perfusion conditions such as pressure, duration, and oxygenation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Neurosciences
Ji-fei Liu, Gang Su, Li-xia Chen, Juan-ping Zhou, Juan Gao, Jia-jia Zhang, Qiong-hui Wu, Wei Chen, De-yi Chen, Zhen-chang Zhang
Summary: This study investigated the beneficial effects and mechanisms of action of irisin in response to cerebral ischemia-reperfusion injury (CIRI). Irisin improved cerebral function, reduced cerebral infarct volume, protected neuronal cells against apoptosis, and alleviated oxidative stress through the prevention of mitochondrial fission, increased mitochondrial fusion, and activation of the PI3K/AKT/mTOR axis. Irisin is identified as a much-needed therapeutic for CIRI.
MOLECULAR NEUROBIOLOGY
(2023)
Article
Engineering, Biomedical
Xiaoping Zhang, Yage Sun, Rong Yang, Bo Liu, Yang Liu, Jianhai Yang, Wenguang Liu
Summary: In this study, a mitochondria-targeted nanomicelle was designed for the treatment of myocardial ischemia-reperfusion injury. The nanomicelle was encapsulated into a pH/ROS dual responsive injectable hydrogel for controllable drug delivery. The treatment effectively restored mitochondrial function and attenuated oxidative stress in a rat model.
Article
Biochemistry & Molecular Biology
Maija Dambrova, Coert J. Zuurbier, Vilmante Borutaite, Edgars Liepinsh, Marina Makrecka-Kuka
Summary: The heart is highly flexible in its metabolism and mitochondria play a crucial role in oxidative phosphorylation and heart function. ROS production pathways during ischemia/reperfusion involve glucose, fatty acids, and the Krebs cycle, with strategies available to modulate substrate accumulation for ROS production mitigation.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Biochemistry & Molecular Biology
Panagiotis Chronopoulos, Caroline Manicam, Jenia Kouchek Zadeh, Panagiotis Laspas, Johanna Charlotte Unkrig, Marie Luise Goebel, Aytan Musayeva, Norbert Pfeiffer, Matthias Oelze, Andreas Daiber, Huige Li, Ning Xia, Adrian Gericke
Summary: This study demonstrates that resveratrol has a protective effect against ischemia-reperfusion injury in the murine retina, reducing the loss of retinal ganglion cells and endothelial dysfunction of retinal blood vessels. This protective effect may be achieved by suppressing upregulation of nitric oxide synthase 2 and alleviating nitro-oxidative stress.
Review
Biochemistry & Molecular Biology
Pasquale Pagliaro, Claudia Penna
Summary: Myocardial ischemia-reperfusion injury (MIRI) is caused by various mechanisms, including ROS production, altered cellular osmolarity, and inflammatory response. Calcium overload, altered oxygen levels, and mitochondrial ROS are also involved, leading to the opening of mPTP. NLRP3 inflammasome priming and activation play a role in these processes and are associated with cell death and endothelial dysfunction. ROS inhibitors and NLRP3 inhibitors have been studied as potential therapeutic agents in ischemic heart disease, but further research is needed to confirm their clinical use.
Article
Chemistry, Multidisciplinary
Liping Wang, Shuwen Qiu, Xi Li, Yabing Zhang, Minfeng Huo, Jianlin Shi
Summary: Ischemic heart disease is a major cause of death worldwide. This study focuses on the synthesis of tannic acid-assembled tetravalent cerium nanocatalysts for the treatment of ischemia/reperfusion injury. The nanocatalysts effectively rescue cardiomyocytes from oxidative stress and reduce myocardial infarct area in a murine model. This research highlights the potential of nanocatalytic metal complexes as a therapeutic approach for ischemic heart diseases.
ANGEWANDTE CHEMIE-INTERNATIONAL EDITION
(2023)
Article
Immunology
Nan-Nan Liang, Ying Zhao, Yue-Yue Guo, Zhi-Hui Zhang, Lan Gao, De-Xin Yu, De-Xiang Xu, Shen Xu
Summary: This study found that mitochondria-derived reactive oxygen species (ROS) contribute to renal cell ferroptosis during lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Inhibition of ferroptosis and scavenging of mitochondrial ROS with specific inhibitors, ferrostatin-1 and MitoQ, respectively, attenuated renal lipid peroxidation, ferroptosis-characteristic mitochondrial damage, and renal cell death. These findings suggest that mitochondria-targeted antioxidants may be potential therapeutic agents for sepsis-induced AKI.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Shuangyu Lv, Huiyang Liu, Honggang Wang
Summary: Ischemia/reperfusion (I/R) injury is characterized by limited blood supply to organs followed by restoration of blood flow and reoxygenation. The interaction between autophagy and the NLRP3 inflammasome plays a crucial role in I/R injury, but the specific mechanisms are not fully understood and require further research for clarification.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Critical Care Medicine
Joseph M. Wider, Erin Gruley, Paul T. Morse, Junmei Wan, Icksoo Lee, Anthony R. Anzell, Garrett M. Fogo, Jennifer Mathieu, Gerald Hish, Brian O'Neil, Robert W. Neumar, Karin Przyklenk, Maik Huettemann, Thomas H. Sanderson
Summary: Mitochondrial dysfunction is a key factor in brain injury following cardiac arrest, and therapies targeting this dysfunction, such as near-infrared light, show promise in reducing brain injury and improving neurological outcomes. Studies on isolated porcine brain cytochrome c oxidase and cultured primary neurons demonstrate that NIR can modulate mitochondria to reduce injury mechanisms. Translational porcine models of cardiac arrest and CPR further show that transcranial NIR treatment improves neurological deficits and reduces brain injury post-resuscitation.
Article
Biochemistry & Molecular Biology
Di Ren, Zhibin He, Julia Fedorova, Jingwen Zhang, Elizabeth Wood, Xiang Zhang, David E. Kang, Ji Li
Summary: Sesn2, a stress-inducible protein, declines with aging in the heart. Lack of Sesn2 results in cardiac aging-like dysfunction and intolerance to ischemia reperfusion stress. Sesn2 deficiency impairs mitochondrial function and affects oxidative phosphorylation complex activity, impacting the maintenance of cardiac mitochondrial integrity.
Article
Biochemistry & Molecular Biology
Ping Pang, Wei Si, Han Wu, Jiaming Ju, Kuiwu Liu, Chunlei Wang, Yingqiong Jia, Hongtao Diao, Linghua Zeng, Weitao Jiang, Yang Yang, Yuting Xiong, Xue Kong, Zhengwei Zhang, Feng Zhang, Jinglun Song, Ning Wang, Baofeng Yang, Yu Bian
Summary: YTHDF2 affects myocardial ischemia-reperfusion injury by regulating RNA stability. Silencing YTHDF2 protects cardiac function and reduces infarct size, while overexpressing YTHDF2 exacerbates pathological processes. RNA analysis reveals that YTHDF2 recognizes m6A modification sites to promote the degradation of SLC7A11. Inhibition of SLC7A11 impairs heart function, increases infarct size, and the release of LDH. These findings provide novel potential therapeutic targets for treating ischemic cardiac diseases.
ANTIOXIDANTS & REDOX SIGNALING
(2023)
Article
Biochemistry & Molecular Biology
Li Ma, Na Zhou, Huikang Tao, Hao Zhou, Ying Tan, Weidan Chen, Fan Cao, Xinxin Chen
Summary: This study investigated the impact of TMBIM6 and PS2 on mitochondrial homeostasis during acute reperfusion injury. It was found that myocardial post-ischemic reperfusion stress disrupted mitochondrial integrity, leading to cardiac dysfunction and cardiomyocyte death, which could be prevented by sufficient expression of TMBIM6. Furthermore, TMBIM6 directly bound to PS2 and promoted its post-transcriptional degradation, thereby reducing reperfusion-induced mitochondrial damage. These findings suggest that TMBIM6 and PS2 are promising therapeutic targets for the treatment of cardiac reperfusion damage.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2023)