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
Biochemistry & Molecular Biology
Jacqueline Heger, Tamara Szabados, Paulin Brosinsky, Peter Bencsik, Peter Ferdinandy, Rainer Schulz
Summary: The knockout of monoamine oxidase (MAO)-B specifically in cardiomyocytes reduces myocardial ischemia/reperfusion (I/R) injury in vitro. In this study, the researchers investigated the impact of MAO-B knockout on myocardial infarction (MI) following I/R in male and female mice. They found that MAO-B knockout protected male mice against MI, but had no effect on infarct size in female mice.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Maxime Schleef, Margaux Rozes, Bruno Pillot, Gabriel Bidaux, Fitsum Guebre-Egziabher, Laurent Juillard, Delphine Baetz, Sandrine Lemoine
Summary: This study aimed to investigate the effect of CsA preconditioning on kidney and mitochondrial functions. The results showed that CsA significantly improved renal function and mitochondrial functions, while the use of Hsp70 inhibitor abolished the protection afforded by CsA. In vitro experiments demonstrated that Hsp70 modulation could protect kidneys from ischemia reperfusion injury by regulating mitochondrial functions. This pathway may be targeted by drugs to provide new therapeutics for improving renal function.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Cardiac & Cardiovascular Systems
Hector Chapoy Villanueva, Jae Hwi Sung, Jackie A. Stevens, Michael J. Zhang, Peyton M. Nelson, Lalitha S. Denduluri, Feng Feng, Timothy D. O'Connell, DeWayne Townsend, Julia C. Liu
Summary: Transport of Ca2+ into mitochondria through the mitochondrial Ca2+ uniporter complex is essential for ATP production, but excessive Ca2+ can be detrimental. Short-term deletion of the regulatory protein EMRE in the heart resulted in impaired Ca2+ uptake, attenuated ATP production, and improved cardiac function in an I/R model. However, long-term EMRE loss led to similar impairment in Ca2+ handling and function, but loss of protection against I/R injury. These findings suggest that long-term absence of EMRE restores susceptibility to I/R, despite impaired bioenergetic response.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2023)
Article
Multidisciplinary Sciences
Noemi Daradics, Gergo Horvath, Laszlo Tretter, Agnes Paal, Andras Fulop, Andras Budai, Attila Szijarto
Summary: Depletion of CypD improves mitochondrial function following ALPPS and enhances liver growth.
Article
Plant Sciences
Yuantao Han, Yuanyuan Cheng, Li-Wen Tian
Summary: The protective effects of 22,25-epoxylanostane triterpenoids against OGD/R-induced myocardial injury were observed. Synthesis of 20 22,25-epoxylanostane triterpenoids was conducted, and compounds 13 and 22 showed potential protective activity against OGD/R-induced injury.
JOURNAL OF NATURAL PRODUCTS
(2023)
Article
Biochemistry & Molecular Biology
Jacqueline Heger, Christine Hirschhaeuser, Julia Bornbaum, Akylbek Sydykov, Astrid Dempfle, Andre Schneider, Thomas Braun, Klaus-Dieter Schlueter, Rainer Schulz
Summary: The creation of MAO-B knockout mice demonstrates that the lack of cardiomyocyte MAO-B can protect the heart from I/R injury and reduce infarct size.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Chemistry, Multidisciplinary
Zelin Chen, Xu Tan, Taotao Jin, Yu Wang, Linyong Dai, Gufang Shen, Can Zhang, Langfan Qu, Lei Long, Chongxing Shen, Xiaohui Cao, Jianwu Wang, Huijuan Li, Xiaofeng Yue, Chunmeng Shi
Summary: This study presents the potential of near infrared dye IR-780 for monitoring and protecting ischemic myocardium from injury. IR-780 selectively enters cardiomyocytes in at-risk heart tissues and can preconditon or administer timely to protect against cell death, myocardial remodeling, and heart failure induced by ischemia and oxidative stress. The dye binds to F0F1-ATP synthase in cardiomyocytes, decreases mitochondrial membrane potential, and slows down mitochondrial energy metabolism, leading to a quiescent mitochondria state and inhibition of mitochondrial permeability transition pore. Moderating mitochondrial function depression could be a targeted approach for developing cardioprotective reagents.
Review
Biochemistry & Molecular Biology
Jirapong Vongsfak, Wasana Pratchayasakul, Nattayaporn Apaijai, Tanat Vaniyapong, Nipon Chattipakorn, Siriporn C. Chattipakorn
Summary: Cerebral ischemia and reperfusion injury can lead to poor oxygen supply, brain infarction, and an imbalance in mitochondrial dynamics, which plays a crucial role in cell survival and infarct area size regulation. Understanding and regulating mitochondrial dynamics may help prevent or treat cerebral injury.
Article
Cardiac & Cardiovascular Systems
Olga M. Rusiecka, Filippo Molica, Morten S. Nielsen, Axel Tollance, Sandrine Morel, Maud Frieden, Marc Chanson, Kerstin Boengler, Brenda R. Kwak
Summary: This study found that deletion of the Pannexin1 (Panx1) gene in cardiac endothelial cells can alleviate cardiac ischaemia/reperfusion (I/R) injury and improve left ventricular function recovery. This cardioprotective effect seems to be mediated through its influence on cardiac mitochondria rather than reducing the inflammatory response. Therefore, Panx1 may represent a new target for controlling cardiac reperfusion damage.
CARDIOVASCULAR RESEARCH
(2023)
Article
Cardiac & Cardiovascular Systems
Chantal Eickelmann, Helmut Raphael Lieder, Sharaf-Eldin Shehada, Matthias Thielmann, Gerd Heusch, Petra Kleinbongard
Summary: Mitochondrial function is critical for myocardial ischemia-reperfusion injury and cardioprotection. Measuring mitochondrial function in permeabilized cardiac tissue can reflect mitochondrial dysfunction following ischemia-reperfusion.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Rene Ferrera, Marie Vedere, Megane Lo-Grasso, Lionel Augeul, Christophe Chouabe, Gabriel Bidaux, Delphine Baetz
Summary: This study aimed to evaluate the protective effects of postconditioning on DCD hearts. The results showed that CsA and POST could reduce necrosis and improve heart function. However, the efficacy of POST was lost if delayed beyond 3 minutes of reperfusion, while CsA treatment remained effective even if applied after a delay. Delayed CsA application correlated with better functional recovery and higher mitochondrial respiratory index, suggesting the crucial role of MPTP in delayed protection of DCD hearts.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Yunxia Liu, Meina Li, Meihua Sun, Yaoting Zhang, Xuan Li, Wanqing Sun, Nanhu Quan
Summary: Sestrin2 (Sesn2) is a stress-inducible protein that plays a critical role in responding to ischemic stress by reducing the generation of reactive oxygen species (ROS). Rescue of Sesn2 levels in Sesn2 KO hearts improved cardiac function, ameliorated ROS generation, and improved cardiomyocyte contractile function under ischemia and reperfusion. Overall, these findings highlight the role of Sesn2 as an endogenous antioxidant in maintaining intracellular redox homeostasis during ischemic stress.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Medicine, Research & Experimental
Tong Li, Houshuai Zeng, Wenjing Xian, Hongxing Cai, Jianbo Zhang, Shiji Zhou, Yingxue Yang, Min Luo, Peng Zhu
Summary: This study found that Maresin1 (MaR1) can reduce liver macrophage pyroptosis by reducing mitochondrial damage, thereby alleviating liver ischemia-reperfusion (I/R) injury. MaR1 inhibits liver macrophage pyroptosis by protecting mitochondria. Finally, it was found that MaR1 exerts mitochondrial protective effects through activation of its nuclear receptor RORa and the PI3K/AKT signaling pathway.
JOURNAL OF TRANSLATIONAL MEDICINE
(2023)
Review
Pharmacology & Pharmacy
Mahmood S. Mozaffari
Summary: The SGK family of proteins includes three paralogs, with SGK-1 being the most studied. SGK-1 plays a crucial role in regulating cell survival and proliferation, and also influences the pathogenesis of organ diseases. Therapeutic modulation of SGK-1 could potentially benefit conditions associated with ischemia-reperfusion injury.
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
(2023)