TY - JOUR AU - Bielanin, J.P. AU - Metwally, S.A.H. AU - Paruchuri, S.S. AU - Sun, D. TI - An overview of mild traumatic brain injuries and emerging therapeutic targets JF - NEUROCHEMISTRY INTERNATIONAL J2 - NEUROCHEM INT VL - 172 PY - 2024 SN - 0197-0186 DO - 10.1016/j.neuint.2023.105655 UR - https://m2.mtmt.hu/api/publication/34499054 ID - 34499054 N1 - Export Date: 12 January 2024 CODEN: NEUID Correspondence Address: Sun, D.; Department of Neurology, 7016 Biomedical Science Tower-3, 3501 Fifth Ave., United States; email: sund@upmc.edu LA - English DB - MTMT ER - TY - JOUR AU - Du, X. AU - Zeng, Q. AU - Luo, Y. AU - He, L. AU - Zhao, Y. AU - Li, N. AU - Han, C. AU - Zhang, G. AU - Liu, W. TI - Application research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction JF - MITOCHONDRION J2 - MITOCHONDRION VL - 75 PY - 2024 SN - 1567-7249 DO - 10.1016/j.mito.2024.101846 UR - https://m2.mtmt.hu/api/publication/34692792 ID - 34692792 N1 - School of Medicine and Life Sciences, Chengdu University of Traditional Chinese Medicine, Sichuan Province, Chengdu, 611137, China Key Laboratory of Reproductive Medicine, Sichuan Provincial Maternity and Child Health Care Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, 610045, China Biology Major, College of Natural Sciences, The University of Texas at Austin, Austin, TX 78712, United States Joint Laboratory of Reproductive Medicine, SCU-CUHK, Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, 610041, China School of Clinical Laboratory Medicine, Chengdu Medical College, Chengdu, 610083, China Export Date: 28 February 2024 CODEN: MITOC Correspondence Address: Zhang, G.; Key Laboratory of Reproductive Medicine, China; email: guohuizhang1992@163.com LA - English DB - MTMT ER - TY - JOUR AU - Seman, A. AU - Chandra, P.K. AU - Byrum, S.D. AU - Mackintosh, S.G. AU - Gies, A.J. AU - Busija, D.W. AU - Rutkai, I. TI - Targeting mitochondria in the aged cerebral vasculature with SS-31, a proteomic study of brain microvessels JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 45 PY - 2023 IS - 5 SP - 2951 EP - 2965 PG - 15 SN - 2509-2715 DO - 10.1007/s11357-023-00845-y UR - https://m2.mtmt.hu/api/publication/34072601 ID - 34072601 N1 - Department of Pharmacology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, United States Tulane Brain Institute, Tulane University, 200 Flower Hall, New Orleans, LA 70118, United States Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, 4301 West Markham Street, Little Rock, AR 72205, United States Cited By :1 Export Date: 28 February 2024 Correspondence Address: Rutkai, I.; Department of Pharmacology, 1430 Tulane Avenue, United States; email: irutkai@tulane.edu AB - Cognitive impairment and dementias during aging such as Alzheimer’s disease are linked to functional decline and structural alterations of the brain microvasculature. Although mechanisms leading to microvascular changes during aging are not clear, loss of mitochondria, and reduced efficiency of remaining mitochondria appear to play a major role. Pharmacological agents, such as SS-31, which target mitochondria have been shown to be effective during aging and diseases; however, the benefit to mitochondrial- and non-mitochondrial proteins in the brain microvasculature has not been examined. We tested whether attenuation of aging-associated changes in the brain microvascular proteome via targeting mitochondria represents a therapeutic option for the aging brain. We used aged male (> 18 months) C57Bl6/J mice treated with a mitochondria-targeted tetrapeptide, SS-31, or vehicle saline. Cerebral blood flow (CBF) was determined using laser speckle imaging during a 2-week treatment period. Then, isolated cortical microvessels (MVs) composed of end arterioles, capillaries, and venules were used for Orbitrap Eclipse Tribrid mass spectrometry. CBF was similar among the groups, whereas bioinformatic analysis revealed substantial differences in protein abundance of cortical MVs between SS-31 and vehicle. We identified 6267 proteins, of which 12% were mitochondria-associated. Of this 12%, 107 were significantly differentially expressed and were associated with oxidative phosphorylation, metabolism, the antioxidant defense system, or mitochondrial dynamics. Administration of SS-31 affected many non-mitochondrial proteins. Our findings suggest that mitochondria in the microvasculature represent a therapeutic target in the aging brain, and widespread changes in the proteome may underlie the rejuvenating actions of SS-31 in aging. © 2023, The Author(s). LA - English DB - MTMT ER - TY - JOUR AU - Cen, J. AU - Zhang, R. AU - Zhao, T. AU - Zhang, X. AU - Zhang, C. AU - Cui, J. AU - Zhao, K. AU - Duan, S. AU - Guo, Y. TI - A Water-Soluble Quercetin Conjugate with Triple Targeting Exerts Neuron-Protective Effect on Cerebral Ischemia by Mitophagy Activation JF - ADVANCED HEALTHCARE MATERIALS J2 - ADV HEALTHC MATER VL - 11 PY - 2022 IS - 22 SN - 2192-2640 DO - 10.1002/adhm.202200817 UR - https://m2.mtmt.hu/api/publication/33141784 ID - 33141784 N1 - Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China Key Laboratory of Natural Medicine and Immune Engineering, School of Pharmacy, Henan University, Kaifeng, 475004, China Institute for Innovative Drug Design and Evaluation, School of Pharmacy, Henan University, Kaifeng, 475004, China School of Chemistry and Chemical Engineering, Frontiers Science Center for Transformative Molecules, Shanghai Key Laboratory for Molecular Engineering of Chiral Drugs, Shanghai Jiao Tong University, Shanghai, 200240, China Henan International Joint Laboratory of Chinese Medicine Efficacy, Henan University, Kaifeng, 475004, China Engineering Research Center for Gynecological Oncology Nanomedicine of Henan Province, Zhengzhou, 450003, China Cited By :9 Export Date: 28 February 2024 Correspondence Address: Guo, Y.; Henan Provincial People's Hospital, China; email: yuqiguo@zzu.edu.cn Correspondence Address: Duan, S.; Key Laboratory of Natural Medicine and Immune Engineering, China; email: sduan@henu.edu.cn LA - English DB - MTMT ER - TY - JOUR AU - Zhang, Jia-ming AU - Jing, Yao AU - Wang, Kun AU - Jiao, Jian-Tong AU - Xu, Jin-yu AU - Shi, Jing AU - Ji, Dong-dong AU - Lu, Shou-rong AU - Li, Xiang-dong AU - Zhang, Yun AU - Cao, Xiao-dong TI - Inhibition of Heat Shock Protein 90 Attenuates the Damage of Blood-Brain Barrier Integrity in Traumatic Brain Injury Mouse Model JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2022 PY - 2022 SN - 1942-0900 DO - 10.1155/2022/5585384 UR - https://m2.mtmt.hu/api/publication/32919195 ID - 32919195 N1 - Funding Agency and Grant Number: Top Talent Support Program for young and middle-aged people of Wuxi Health Committee [HB2020019]; Young Project of Wuxi Health Committee [Q201914]; Wuxi Health Planning Commission Project [MS201603]; Natural Science Foundation of Shandong Province [ZR2020MH141]; Shandong Post-Doctoral Innovation Project [202003063] Funding text: This research was supported by the Top Talent Support Program for young and middle-aged people of Wuxi Health Committee (HB2020019), Young Project of Wuxi Health Committee (Q201914), Wuxi Health Planning Commission Project (MS201603), Natural Science Foundation of Shandong Province (ZR2020MH141), and Shandong Post-Doctoral Innovation Project (202003063). LA - English DB - MTMT ER - TY - JOUR AU - Bhatti, Jasvinder Singh AU - Tamarai, Kavya AU - Kandimalla, Ramesh AU - Manczak, Maria AU - Yin, Xiangling AU - Ramasubramanian, Bhagavathi AU - Sawant, Neha AU - Pradeepkiran, Jangampalli Adi AU - Vijayan, Murali AU - Kumar, Subodh AU - Reddy, P. Hemachandra TI - Protective effects of a mitochondria-targeted small peptide SS31 against hyperglycemia-induced mitochondrial abnormalities in the liver tissues of diabetic mice, Tallyho/JngJ mice JF - MITOCHONDRION J2 - MITOCHONDRION VL - 58 PY - 2021 SP - 49 EP - 58 PG - 10 SN - 1567-7249 DO - 10.1016/j.mito.2021.02.007 UR - https://m2.mtmt.hu/api/publication/32051058 ID - 32051058 N1 - Department of Human Genetics and Molecular Medicine, School of Health Sciences, Central University of Punjab, Bathinda, India Department of Biotechnology, Sri Guru Gobind Singh College, Chandigarh, India Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Department of Biochemistry, Kakatiya Medical College, Warangal, Telangana 506007, India Applied Biology, CSIR-Indian Institute of Technology, Uppal Road, Tarnaka, Hyderabad, Telangana 500007, India Internal Medicine Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Pharmacology & Neuroscience Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States Cited By :15 Export Date: 28 February 2024 CODEN: MITOC Correspondence Address: Reddy, P.H.; Garrison Institute on Aging, 3601 4th Street, MS 9424, United States; email: hemachandra.reddy@ttuhsc.edu AB - Type 2 Diabetes mellitus (T2DM) has become a major public health issue associated with a high risk of late-onset Alzheimer's disease (LOAD). Mitochondrial dysfunction is one of the molecular events that occur in the LOAD pathophysiology. The present study was planned to investigate the molecular alterations induced by hyperglycemia in the mitochondria of diabetic mice and further explore the possible ameliorative role of the mitochondria-targeted small peptide, SS31 in diabetic mice. For this purpose, we used a polygenic mouse model of type 2 diabetes, TALLYHO/JngJ (TH), and nondiabetic, SWR/J mice strains. The diabetic status in TH mice was confirmed at 8 weeks of age. The 24 weeks old experimental animals were segregated into three groups: Non-diabetic controls (SWR/J mice), diabetic (TH mice) and, SS31 treated diabetic TH mice. The mRNA and protein expression levels of mitochondrial proteins were investigated in all the study groups in the liver tissues using qPCR and immunoblot analysis. Also, the mitochondrial functions including H2O2 production, ATP generation, and lipid peroxidation were assessed in all the groups. Mitochondrial dysfunction was observed in TH mice as evident by significantly elevated H2O2 production, lipid peroxidation, and reduced ATP production. The mRNA expression and Western blot analysis of mitochondrial dynamics (Drp1 and Fis1 - fission; Mfn1, Mfn2, and Opa1 -fusion), and biogenesis (PGC-1 alpha, Nrf1, Nrf2, and TFAM) genes were significantly altered in diabetic TH mice. Furthermore, SS31 treatment significantly reduced the mitochondrial abnormalities and restore mitochondrial functions in diabetic TH mice. LA - English DB - MTMT ER - TY - JOUR AU - Kirkman, Danielle L. AU - Robinson, Austin T. AU - Rossman, Matthew J. AU - Seals, Douglas R. AU - Edwards, David G. TI - Mitochondrial contributions to vascular endothelial dysfunction, arterial stiffness, and cardiovascular diseases JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 320 PY - 2021 IS - 5 SP - H2080 EP - H2100 PG - 21 SN - 0363-6135 DO - 10.1152/ajpheart.00917.2020 UR - https://m2.mtmt.hu/api/publication/32097756 ID - 32097756 N1 - Department of Kinesiology and Health Sciences, Virginia Commonwealth University, Richmond, VA, United States School of Kinesiology, Auburn University, Auburn, AL, United States Department of Integrative Physiology, University of Colorado, Boulder, CO, United States Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE, United States Cited By :41 Export Date: 28 February 2024 CODEN: AJPPD Correspondence Address: Edwards, D.G.; Department of Kinesiology and Applied Physiology, United States; email: dge@udel.edu AB - Cardiovascular disease (CVD) affects one in three adults and remains the leading cause of death in America. Advancing age is a major risk factor for CVD. Recent plateaus in CVD-related mortality rates in high-income countries after decades of decline highlight a critical need to identify novel therapeutic targets and strategies to mitigate and manage the risk of CVD development and progression. Vascular dysfunction, characterized by endothelial dysfunction and large elastic artery stiffening, is independently associated with an increased CVD risk and incidence and is therefore an attractive target for CVD prevention and management. Vascular mitochondria have emerged as an important player in maintaining vascular homeostasis. As such, age- and disease-related impairments in mitochondrial function contribute to vascular dysfunction and consequent increases in CVD risk. This review outlines the role of mitochondria in vascular function and discusses the ramifications of mitochondrial dysfunction on vascular health in the setting of age and disease. The adverse vascular consequences of increased mitochondrial-derived reactive oxygen species, impaired mitochondria! quality control, and defective mitochondria! calcium cycling are emphasized, in particular. Current evidence for both lifestyle and pharmaceutical mitochondrial-targeted strategies to improve vascular function is also presented. LA - English DB - MTMT ER - TY - JOUR AU - Brand, M.D. TI - Riding the tiger–physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix JF - CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY J2 - CRIT REV BIOCHEM MOL VL - 55 PY - 2020 IS - 6 SP - 592 EP - 661 PG - 70 SN - 1040-9238 DO - 10.1080/10409238.2020.1828258 UR - https://m2.mtmt.hu/api/publication/31666293 ID - 31666293 N1 - Cited By :54 Export Date: 21 February 2024 CODEN: CRBBE Correspondence Address: Brand, M.D.; Buck Institute for Research on AgingUnited States; email: mbrand@buckinstitute.org Chemicals/CAS: hydrogen peroxide, 7722-84-1; superoxide, 11062-77-4; thioredoxin, 52500-60-4; Antioxidants; Hydrogen Peroxide; Reactive Oxygen Species; Superoxides; Thioredoxins Funding details: Buck Institute for Research on Aging Funding text 1: Work in my laboratory is supported by Calico Life Sciences LLC (South San Francisco, CA) and the Buck Institute for Research on Aging (Novato, CA). AB - Elevated mitochondrial matrix superoxide and/or hydrogen peroxide concentrations drive a wide range of physiological responses and pathologies. Concentrations of superoxide and hydrogen peroxide in the mitochondrial matrix are set mainly by rates of production, the activities of superoxide dismutase-2 (SOD2) and peroxiredoxin-3 (PRDX3), and by diffusion of hydrogen peroxide to the cytosol. These considerations can be used to generate criteria for assessing whether changes in matrix superoxide or hydrogen peroxide are both necessary and sufficient to drive redox signaling and pathology: is a phenotype affected by suppressing superoxide and hydrogen peroxide production; by manipulating the levels of SOD2, PRDX3 or mitochondria-targeted catalase; and by adding mitochondria-targeted SOD/catalase mimetics or mitochondria-targeted antioxidants? Is the pathology associated with variants in SOD2 and PRDX3 genes? Filtering the large literature on mitochondrial redox signaling using these criteria highlights considerable evidence that mitochondrial superoxide and hydrogen peroxide drive physiological responses involved in cellular stress management, including apoptosis, autophagy, propagation of endoplasmic reticulum stress, cellular senescence, HIF1α signaling, and immune responses. They also affect cell proliferation, migration, differentiation, and the cell cycle. Filtering the huge literature on pathologies highlights strong experimental evidence that 30-40 pathologies may be driven by mitochondrial matrix superoxide or hydrogen peroxide. These can be grouped into overlapping and interacting categories: metabolic, cardiovascular, inflammatory, and neurological diseases; cancer; ischemia/reperfusion injury; aging and its diseases; external insults, and genetic diseases. Understanding the involvement of mitochondrial matrix superoxide and hydrogen peroxide concentrations in these diseases can facilitate the rational development of appropriate therapies. LA - English DB - MTMT ER - TY - JOUR AU - Forte, M. AU - Stanzione, R. AU - Cotugno, M. AU - Bianchi, F. AU - Marchitti, S. AU - Rubattu, S. TI - Vascular ageing in hypertension: Focus on mitochondria JF - MECHANISMS OF AGEING AND DEVELOPMENT J2 - MECH AGEING DEV VL - 189 PY - 2020 SN - 0047-6374 DO - 10.1016/j.mad.2020.111267 UR - https://m2.mtmt.hu/api/publication/31349700 ID - 31349700 N1 - IRCCS Neuromed, Via Atinense, 18, Pozzilli, IS 86077, Italy Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University of Rome, Rome, 00189, Italy Cited By :15 Export Date: 28 February 2024 CODEN: MAGDA Correspondence Address: Rubattu, S.; Department of Clinical and Molecular Medicine, Ospedale S. Andrea, Italy; email: rubattu.speranza@neuromed.it LA - English DB - MTMT ER - TY - JOUR AU - Jiang, Qian AU - Yin, Jie AU - Chen, Jiashun AU - Ma, Xiaokang AU - Wu, Miaomiao AU - Liu, Gang AU - Yao, Kang AU - Tan, Bie AU - Yin, Yulong TI - Mitochondria-Targeted Antioxidants: A Step towards Disease Treatment JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2020 PY - 2020 PG - 18 SN - 1942-0900 DO - 10.1155/2020/8837893 UR - https://m2.mtmt.hu/api/publication/31813255 ID - 31813255 N1 - Animal Nutritional Genome and Germplasm Innovation Research Center, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China Key Laboratory of Feed Biotechnology, The Ministry of Agriculture and Rural Affairs of the People's Republic of China, Beijing, 100081, China College of Bioscience and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China Laboratory of Animal Nutritional Physiology and Metabolic Process, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, Hunan, 410125, China Cited By :64 Export Date: 28 February 2024 Correspondence Address: Yin, J.; Animal Nutritional Genome and Germplasm Innovation Research Center, China; email: yinjie2014@126.com Correspondence Address: Tan, B.; Animal Nutritional Genome and Germplasm Innovation Research Center, China; email: bietan@hunau.edu.cn AB - Mitochondria are the main organelles that produce adenosine 5 '-triphosphate (ATP) and reactive oxygen species (ROS) in eukaryotic cells and meanwhile susceptible to oxidative damage. The irreversible oxidative damage in mitochondria has been implicated in various human diseases. Increasing evidence indicates the therapeutic potential of mitochondria-targeted antioxidants (MTAs) for oxidative damage-associated diseases. In this article, we introduce the advantageous properties of MTAs compared with the conventional (nontargeted) ones, review different mitochondria-targeted delivery systems and antioxidants, and summarize their experimental results for various disease treatments in different animal models and clinical trials. The combined evidence demonstrates that mitochondrial redox homeostasis is a potential target for disease treatment. Meanwhile, the limitations and prospects for exploiting MTAs are discussed, which might pave ways for further trial design and drug development. LA - English DB - MTMT ER - TY - JOUR AU - Lazzarino, G. AU - Amorini, A.M. AU - Barnes, N.M. AU - Bruce, L. AU - Mordente, A. AU - Lazzarino, G. AU - Di, Pietro V. AU - Tavazzi, B. AU - Belli, A. AU - Logan, A. TI - Low molecular weight dextran sulfate (Ilb® ) administration restores brain energy metabolism following severe traumatic brain injury in the rat JF - ANTIOXIDANTS J2 - ANTIOXIDANTS-BASEL VL - 9 PY - 2020 IS - 9 PG - 18 SN - 2076-3921 DO - 10.3390/antiox9090850 UR - https://m2.mtmt.hu/api/publication/31666292 ID - 31666292 N1 - UniCamillus-Saint Camillus International University of Health Sciences, Via di Sant’Alessandro 8, Rome, 00131, Italy Department of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Via S. Sofia 97, Catania, 95123, Italy National Institute for Health Research Surgical Reconstruction and Microbiology Research Centre, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15 2TH, United Kingdom Institute of Clinical Sciences, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom Tikomed AB, Viken, 26303, Sweden Department of Basic Biotechnological Sciences, Intensive and Perioperative Clinics, Catholic University of the Sacred Heart of Rome, Largo F. Vito 1, Rome, 00168, Italy Department of Laboratory Sciences and Infectious Disease, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy Neurotrauma and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom Axolotl Consulting Ltd, Droitwich, Worcestershire, WR9 0JS, United Kingdom Cited By :10 Export Date: 1 February 2024 Correspondence Address: Lazzarino, G.; Department of Biomedical and Biotechnological Sciences, Via S. Sofia 97, Italy; email: lazzarig@unict.it Correspondence Address: Di Pietro, V.; National Institute for Health Research Surgical Reconstruction and Microbiology Research Centre, Edgbaston, United Kingdom; email: v.dipietro@bham.ac.uk Correspondence Address: Di Pietro, V.; Neurotrauma and Ophthalmology Research Group, Edgbaston, United Kingdom; email: v.dipietro@bham.ac.uk Correspondence Address: Tavazzi, B.; UniCamillus-Saint Camillus International University of Health Sciences, Via di Sant’Alessandro 8, Italy; email: barbara.tavazzi@unicatt.it Correspondence Address: Tavazzi, B.; Department of Basic Biotechnological Sciences, Largo F. Vito 1, Italy; email: barbara.tavazzi@unicatt.it Correspondence Address: Tavazzi, B.; Department of Laboratory Sciences and Infectious Disease, Largo A. Gemelli 8, Italy; email: barbara.tavazzi@unicatt.it Correspondence Address: Logan, A.; Axolotl Consulting LtdUnited Kingdom; email: a.logan@axolotlconsulting.com LA - English DB - MTMT ER - TY - JOUR AU - Rohani, Leili AU - Machiraju, Pranav AU - Sabouny, Rasha AU - Meng, Guoliang AU - Liu, Shiying AU - Zhao, Tian AU - Iqbal, Fatima AU - Wang, Xuemei AU - Ravandi, Amir AU - Wu, Joseph C. AU - Khan, Aneal AU - Shutt, Timothy AU - Rancourt, Derrick AU - Greenway, Steven C. TI - Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy JF - CANADIAN JOURNAL OF CARDIOLOGY J2 - CAN J CARDIOL VL - 36 PY - 2020 IS - 4 SP - 554 EP - 563 PG - 10 SN - 0828-282X DO - 10.1016/j.cjca.2019.09.021 UR - https://m2.mtmt.hu/api/publication/31349689 ID - 31349689 N1 - Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Department of Physiology and Pathophysiology and Institute of Cardiovascular Sciences, St Boniface Hospital Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, United States Department of Medical Genetics, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta, Canada Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada Cited By :26 Export Date: 28 February 2024 CODEN: CJCAE Correspondence Address: Greenway, S.C.; Section of Cardiology, 28 Oki Drive NW, Canada; email: scgreenw@ucalgary.ca LA - English DB - MTMT ER - TY - JOUR AU - Rutkai, I. AU - Evans, W.R. AU - Bess, N. AU - Salter-Cid, T. AU - Cikic, S. AU - Chandra, P.K. AU - Katakam, P.V.G. AU - Mostany, R. AU - Busija, D.W. TI - Chronic imaging of mitochondria in the murine cerebral vasculature using in vivo two-photon microscopy JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 318 PY - 2020 IS - 6 SP - H1379 EP - H1386 SN - 0363-6135 DO - 10.1152/ajpheart.00751.2019 UR - https://m2.mtmt.hu/api/publication/31349701 ID - 31349701 N1 - Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA, United States Tulane Brain Institute, Tulane University, New Orleans, LA, United States Cited By :6 Export Date: 28 February 2024 CODEN: AJPPD Correspondence Address: Rutkai, I.; Department of Pharmacology, United States; email: irutkai@tulane.edu LA - English DB - MTMT ER - TY - JOUR AU - Song, K. AU - Li, Y. AU - Zhang, H. AU - An, N. AU - Wei, Y. AU - Wang, L. AU - Tian, C. AU - Yuan, M. AU - Sun, Y. AU - Xing, Y. AU - Gao, Y. AU - Santibañez, J.F. TI - Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2020 PY - 2020 SN - 1942-0900 DO - 10.1155/2020/4356386 UR - https://m2.mtmt.hu/api/publication/31607817 ID - 31607817 N1 - Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated, Beijing University of Chinese Medicine, Beijing, 100700, China Guang'An Men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China Cited By :72 Export Date: 28 February 2024 Correspondence Address: Xing, Y.; Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, China; email: xingyanwei12345@163.com AB - The blood-brain barrier (BBB), as a crucial gate of brain-blood molecular exchange, is involved in the pathogenesis of multiple neurological diseases. Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the scavenger system. Since oxidative stress plays a significant role in the production and maintenance of the BBB, the cerebrovascular system is especially vulnerable to it. The pathways that initiate BBB dysfunction include, but are not limited to, mitochondrial dysfunction, excitotoxicity, iron metabolism, cytokines, pyroptosis, and necroptosis, all converging on the generation of ROS. Interestingly, ROS also provide common triggers that directly regulate BBB damage, parameters including tight junction (TJ) modifications, transporters, matrix metalloproteinase (MMP) activation, inflammatory responses, and autophagy. We will discuss the role of oxidative stress-mediated BBB disruption in neurological diseases, such as hemorrhagic stroke, ischemic stroke (IS), Alzheimer's disease (AD), Parkinson's disease (PD), traumatic brain injury (TBI), amyotrophic lateral sclerosis (ALS), and cerebral small vessel disease (CSVD). This review will also discuss the latest clinical evidence of potential biomarkers and antioxidant drugs towards oxidative stress in neurological diseases. A deeper understanding of how oxidative stress damages BBB may open up more therapeutic options for the treatment of neurological diseases. © 2020 Ke Song et al. LA - English DB - MTMT ER - TY - JOUR AU - Zhang, Qi AU - Liu, Su AU - Sun, Li AU - Zhu, Zhenjie AU - Qin, Zhengji AU - Shen, Guangyu TI - Analysis of factors affecting cognitive function in patients with traumatic brain injury JF - Chinese Journal of Nautical Medicine and Hyperbaric Medicine VL - 27 PY - 2020 IS - 4 SP - 427 PG - 5 SN - 1009-6906 DO - 10.3760/cma.j.cn311847-20191209-00374 UR - https://m2.mtmt.hu/api/publication/32686573 ID - 32686573 N1 - Cited By :1 Export Date: 28 February 2024 Correspondence Address: Liu, S.; Medical School of Nantong UniversityChina; email: 327202278@qq.com AB - Objective To analyze the key influencing factors of cognitive function of patients with moderate and severe traumatic brain injury (TBI).Methods The clinical data of 113 patients with moderate and severe TBI admitted to the Department of Rehabilitation Medicine of the Affiliated Hospital of Nantong University from January 1st,2012 to December 31st,2018 were retrospectively reviewed to analyze the factors affecting cognitive function in patients with moderate and severe TBI by using the Mini-Mental State Examination (MMSE) to evaluate the cognitive function of patients at discharge.Results The average age of 113 patients was 52.42 14.20 years old,among whom 74.34% were male and 64.6% of the male patients were injured due to traffic accidents.In the univariate analysis,a total of 8 variables related with MMSE at discharge,including age,history of hypertension,Glasgow coma scale (GCS) at admission,abnormal pupillary reflex at admission,tracheotomy,days of coma,hyperbaric oxygen therapy,and hydrocephalus during hospitalization,with statistically significant differences (P<0.05).Multivariate analysis showed that GCS score at admission,hyperbaric oxygen therapy,days of coma,and age were the independent factors affecting MMSE at discharge,and the differences were statistically significant (P< 0.05).Conclusion GCS score at admission,days of coma,and age can be adopted independently to determine the cognitive function of patients with moderate and severe TBI.Hydrocephalus during hospitalization,history of hypertension,abnormal pupillary reflex at admission,and tracheotomy can be used synthetically to determine the cognitive function.Hyperbaric oxygen therapy can improve the cognitive function. LA - Chinese DB - MTMT ER -