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)
Review
Biochemistry & Molecular Biology
Ivo F. Machado, Carlos M. Palmeira, Anabela P. Rolo
Summary: Liver ischemia-reperfusion injury (LIRI) is a major cause of complications in liver resection and transplantation. Mitochondrial dysfunction is recognized as a hallmark of LIRI and exacerbates cellular injury. Protecting mitochondria through regulation of mitochondrial biogenesis, fission/fusion, and mitophagy can ameliorate LIRI and improve patient outcomes.
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
Cardiac & Cardiovascular Systems
Ana C. M. Omoto, Jussara M. do Carmo, Benjamin Nelson, Nikaela Aitken, Xuemei Dai, Sydney Moak, Elizabeth Flynn, Zhen Wang, Alan J. Mouton, Xuan Li, John E. Hall, Alexandre A. da Silva
Summary: This study found that central nervous system actions of leptin can significantly improve cardiac function and mitochondrial metabolism after myocardial ischemia/reperfusion injury, regardless of sex. These effects are largely independent of cardiac sympathetic innervation.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2022)
Review
Cardiac & Cardiovascular Systems
Magda C. Diaz-Vesga, Ursula Zuniga-Cuevas, Andres Ramirez-Reyes, Nicolas Herrera-Zelada, Ivan Palomo, Roberto Bravo-Sagua, Jaime A. Riquelme
Summary: Despite advances in treating myocardial infarction, limiting infarct size after reperfusion to prevent heart failure remains a challenge, with factors such as comorbidities and experimental models needing to be considered for effective cardioprotection studies. Studies show that current therapeutic strategies may not fully protect the aging heart from myocardial infarction, prompting the need for potential new cardioprotective strategies targeting the aging heart.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
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.
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
Nadezda V. Andrianova, Ljubava D. Zorova, Irina B. Pevzner, Nataliya G. Kolosova, Egor Y. Plotnikov, Dmitry B. Zorov
Summary: Kidney diseases are common among elderly people due to age-related changes in renal tissue. The lack of targeted pharmacotherapies for acute kidney injury (AKI) results in high mortality rates. This study investigated the protective effects of calorie restriction (CR) on ischemic AKI in OXYS rats and found that CR provided significant nephroprotection. Improvements in mitochondrial functioning may be one of the mechanisms for the beneficial effects of CR.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Jingwen Zhang, Zhibin He, Julia Fedorova, Cole Logan, Lauryn Bates, Kayla Davitt, Van Le, Jiayuan Murphy, Melissa Li, Mingyi Wang, Edward G. Lakatta, Di Ren, Ji Li
Summary: SIRT1 and SIRT3 play critical roles in protecting cardiac function against ischemia/reperfusion injury by maintaining mitochondrial homeostasis, particularly mitochondrial dynamics. Deficiency of SIRT1 and SIRT3 results in impaired mitochondrial respiration and contractile function of cardiomyocytes under I/R stress, highlighting their importance in cardiac health.
Article
Biochemistry & Molecular Biology
Maria Bencurova, Terezia Lysikova, Katarina Leskova Majdova, Peter Kaplan, Peter Racay, Jan Lehotsky, Zuzana Tatarkova
Summary: Heart structure and function deteriorate with aging, making the heart more susceptible to ischemia-reperfusion (IR) damage. Maintaining Ca2+ homeostasis is crucial for cardiac contractility. Aging reduces the abundance and function of Ca2+-handling proteins, but the effect of IR on these proteins does not increase with age.
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.
Review
Medicine, Research & Experimental
Yingchao Gong, Jun Lin, Zetao Ma, Mei Yu, Meihui Wang, Dongwu Lai, Guosheng Fu
Summary: The mitochondria-associated membrane (MAM) plays a crucial role in the pathogenesis of cardiac ischemia and reperfusion (I/R) and heart failure. Restoring and maintaining the physiological contact between mitochondria and the endoplasmic reticulum (ER) may improve mitochondrial function, inhibit cell death, and alleviate heart injury and disease development.
Article
Biochemistry & Molecular Biology
Wei Ou, Yu Liang, Yu Qing, Wei Wu, Maodi Xie, Yabing Zhang, Yarong Zhang, Liwei Ji, Haiyang Yu, Tao Li
Summary: The study revealed that hypoxic acclimation (HA) can alleviate cardiac ischemia-reperfusion (I/R) injury by enhancing antioxidative capacity through activation of glucose metabolism, particularly by upregulating the enzyme G6PDH. This cardioprotective effect highlights the potential of HA as a promising strategy against I/R injury, suggesting that O-GlcNAc modification of G6PDH could be a therapeutic target for ischemic heart disease.
Review
Cell Biology
Felipe Salazar-Ramirez, Roberto Ramos-Mondragon, Gerardo Garcia-Rivas
Summary: Ca2+plays a crucial role in mitochondrial function, and the communication between mitochondria and SR is essential for cellular energy production and signaling. The balance between mitochondria and SR maintains normal cellular function, and any imbalance can lead to abnormal excitability of cardiac cells.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Jaganathan Subramani, Venkatesh Kundumani-Sridharan, Rob H. P. Hilgers, Cade Owens, Kumuda C. Das
JOURNAL OF BIOLOGICAL CHEMISTRY
(2016)
Article
Cell Biology
Rob H. P. Hilgers, Venkatesh Kundumani-Sridharan, Jaganathan Subramani, Leon C. Chen, Luis G. Cuello, Nancy J. Rusch, Kumuda C. Das
SCIENCE TRANSLATIONAL MEDICINE
(2017)
Review
Peripheral Vascular Disease
Kumuda C. Das, Venkatesh Kundumani-Sridharan, Jaganathan Subramani
CURRENT HYPERTENSION REPORTS
(2018)
Article
Physiology
Venkat Es H. Kundumani-Sridharan, Jaganathan Subramani, Somasundaram Raghavan, Guru P. Maki, Cade Owens, Trevor Walker, John Wasnick, Steven Idell, Kumuda C. Das
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
(2019)
Article
Cardiac & Cardiovascular Systems
Kumuda C. Das, Harish Muniyappa, Venkatesh Kundumani-Sridharan, Jaganathan Subramani
Summary: Research has shown that cancer cells overexpressing thioredoxin (Trx) exhibit enhanced apoptosis in response to daunomycin, while cells overexpressing redox-inactive mutant Trx were not effectively killed. Furthermore, increased levels of Trx specifically potentiate anthracycline toxicity, but not with other topoisomerase II inhibitors such as etoposide.
CARDIOVASCULAR TOXICOLOGY
(2021)
Article
Hematology
Venkatesh Kundumani-Sridharan, Jaganathan Subramani, Cade Owens, Kumuda C. Das
Summary: The study identified Nrg1 beta as a RIPC factor that interacts with endothelial ErbB2 to prevent degradation and decrease myocardial apoptosis through other molecular pathways. This finding is crucial for understanding the protective mechanism of RIPC.
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Jaganathan Subramani, Venkatesh Kundumani-Sridharan, Kumuda C. Das
Summary: In the context of myocardial ischemia-reperfusion injury, it has been discovered that SG-eNOS undergoes degradation through a specific mechanism, preventing further tissue damage but also causing irreversible loss of eNOS and NO availability.
CIRCULATION RESEARCH
(2021)