@article{MTMT:34499054, title = {An overview of mild traumatic brain injuries and emerging therapeutic targets}, url = {https://m2.mtmt.hu/api/publication/34499054}, author = {Bielanin, J.P. and Metwally, S.A.H. and Paruchuri, S.S. and Sun, D.}, doi = {10.1016/j.neuint.2023.105655}, journal-iso = {NEUROCHEM INT}, journal = {NEUROCHEMISTRY INTERNATIONAL}, volume = {172}, unique-id = {34499054}, issn = {0197-0186}, year = {2024}, eissn = {1872-9754} } @article{MTMT:34692792, title = {Application research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction}, url = {https://m2.mtmt.hu/api/publication/34692792}, author = {Du, X. and Zeng, Q. and Luo, Y. and He, L. and Zhao, Y. and Li, N. and Han, C. and Zhang, G. and Liu, W.}, doi = {10.1016/j.mito.2024.101846}, journal-iso = {MITOCHONDRION}, journal = {MITOCHONDRION}, volume = {75}, unique-id = {34692792}, issn = {1567-7249}, year = {2024}, eissn = {1872-8278} } @article{MTMT:34072601, title = {Targeting mitochondria in the aged cerebral vasculature with SS-31, a proteomic study of brain microvessels}, url = {https://m2.mtmt.hu/api/publication/34072601}, author = {Seman, A. and Chandra, P.K. and Byrum, S.D. and Mackintosh, S.G. and Gies, A.J. and Busija, D.W. and Rutkai, I.}, doi = {10.1007/s11357-023-00845-y}, journal-iso = {GEROSCIENCE}, journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)}, volume = {45}, unique-id = {34072601}, issn = {2509-2715}, abstract = {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).}, keywords = {Mitochondria; Aging; proteomics; Brain microvasculature}, year = {2023}, eissn = {2509-2723}, pages = {2951-2965} } @article{MTMT:33141784, title = {A Water-Soluble Quercetin Conjugate with Triple Targeting Exerts Neuron-Protective Effect on Cerebral Ischemia by Mitophagy Activation}, url = {https://m2.mtmt.hu/api/publication/33141784}, author = {Cen, J. and Zhang, R. and Zhao, T. and Zhang, X. and Zhang, C. and Cui, J. and Zhao, K. and Duan, S. and Guo, Y.}, doi = {10.1002/adhm.202200817}, journal-iso = {ADV HEALTHC MATER}, journal = {ADVANCED HEALTHCARE MATERIALS}, volume = {11}, unique-id = {33141784}, issn = {2192-2640}, year = {2022}, eissn = {2192-2659} } @article{MTMT:32919195, title = {Inhibition of Heat Shock Protein 90 Attenuates the Damage of Blood-Brain Barrier Integrity in Traumatic Brain Injury Mouse Model}, url = {https://m2.mtmt.hu/api/publication/32919195}, author = {Zhang, Jia-ming and Jing, Yao and Wang, Kun and Jiao, Jian-Tong and Xu, Jin-yu and Shi, Jing and Ji, Dong-dong and Lu, Shou-rong and Li, Xiang-dong and Zhang, Yun and Cao, Xiao-dong}, doi = {10.1155/2022/5585384}, journal-iso = {OXID MED CELL LONGEV}, journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY}, volume = {2022}, unique-id = {32919195}, issn = {1942-0900}, year = {2022}, eissn = {1942-0994} } @article{MTMT:32051058, title = {Protective effects of a mitochondria-targeted small peptide SS31 against hyperglycemia-induced mitochondrial abnormalities in the liver tissues of diabetic mice, Tallyho/JngJ mice}, url = {https://m2.mtmt.hu/api/publication/32051058}, author = {Bhatti, Jasvinder Singh and Tamarai, Kavya and Kandimalla, Ramesh and Manczak, Maria and Yin, Xiangling and Ramasubramanian, Bhagavathi and Sawant, Neha and Pradeepkiran, Jangampalli Adi and Vijayan, Murali and Kumar, Subodh and Reddy, P. Hemachandra}, doi = {10.1016/j.mito.2021.02.007}, journal-iso = {MITOCHONDRION}, journal = {MITOCHONDRION}, volume = {58}, unique-id = {32051058}, issn = {1567-7249}, abstract = {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.}, keywords = {DYSFUNCTION; ALZHEIMERS-DISEASE; BETA; antioxidants; DYNAMICS; INSULIN-RESISTANCE; MOUSE MODEL; ATP; BIOGENESIS; CELL BIOLOGY; Type 2 diabetes; mitochondrial dynamics; synaptic degeneration; Oxidative stress; Oxidative stress}, year = {2021}, eissn = {1872-8278}, pages = {49-58}, orcid-numbers = {Kandimalla, Ramesh/0000-0002-3313-4393; Pradeepkiran, Jangampalli Adi/0000-0003-4678-6443; Kumar, Subodh/0000-0003-4705-122X} } @article{MTMT:32097756, title = {Mitochondrial contributions to vascular endothelial dysfunction, arterial stiffness, and cardiovascular diseases}, url = {https://m2.mtmt.hu/api/publication/32097756}, author = {Kirkman, Danielle L. and Robinson, Austin T. and Rossman, Matthew J. and Seals, Douglas R. and Edwards, David G.}, doi = {10.1152/ajpheart.00917.2020}, journal-iso = {AM J PHYSIOL HEART C}, journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY}, volume = {320}, unique-id = {32097756}, issn = {0363-6135}, abstract = {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.}, keywords = {NITRIC-OXIDE; ENDOTHELIUM; physiology; Mitochondria; vascular; Caloric Restriction; ACTIVATED PROTEIN-KINASE; reactive oxygen; flow-mediated dilation; Uncoupling protein-2; REDUCES OXIDATIVE STRESS; Cardiac & Cardiovascular Systems; SUPEROXIDE-PRODUCTION; TARGETED ANTIOXIDANT}, year = {2021}, eissn = {1522-1539}, pages = {H2080-H2100} } @article{MTMT:31666293, title = {Riding the tiger–physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix}, url = {https://m2.mtmt.hu/api/publication/31666293}, author = {Brand, M.D.}, doi = {10.1080/10409238.2020.1828258}, journal-iso = {CRIT REV BIOCHEM MOL}, journal = {CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY}, volume = {55}, unique-id = {31666293}, issn = {1040-9238}, abstract = {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.}, year = {2020}, eissn = {1549-7798}, pages = {592-661} } @article{MTMT:31349700, title = {Vascular ageing in hypertension: Focus on mitochondria}, url = {https://m2.mtmt.hu/api/publication/31349700}, author = {Forte, M. and Stanzione, R. and Cotugno, M. and Bianchi, F. and Marchitti, S. and Rubattu, S.}, doi = {10.1016/j.mad.2020.111267}, journal-iso = {MECH AGEING DEV}, journal = {MECHANISMS OF AGEING AND DEVELOPMENT}, volume = {189}, unique-id = {31349700}, issn = {0047-6374}, year = {2020}, eissn = {1872-6216} } @article{MTMT:31813255, title = {Mitochondria-Targeted Antioxidants: A Step towards Disease Treatment}, url = {https://m2.mtmt.hu/api/publication/31813255}, author = {Jiang, Qian and Yin, Jie and Chen, Jiashun and Ma, Xiaokang and Wu, Miaomiao and Liu, Gang and Yao, Kang and Tan, Bie and Yin, Yulong}, doi = {10.1155/2020/8837893}, journal-iso = {OXID MED CELL LONGEV}, journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY}, volume = {2020}, unique-id = {31813255}, issn = {1942-0900}, abstract = {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.}, keywords = {HEART-FAILURE; OXIDATIVE DNA-DAMAGE; TRAUMATIC BRAIN-INJURY; PENETRATING PEPTIDES; LIPOSOME-BASED CARRIER; MITO-PORTER; PLASTOQUINONE DERIVATIVES; CARDIOLIPIN OXIDATION; INTERRUPT EXECUTION}, year = {2020}, eissn = {1942-0994} } @article{MTMT:31666292, title = {Low molecular weight dextran sulfate (Ilb® ) administration restores brain energy metabolism following severe traumatic brain injury in the rat}, url = {https://m2.mtmt.hu/api/publication/31666292}, author = {Lazzarino, G. and Amorini, A.M. and Barnes, N.M. and Bruce, L. and Mordente, A. and Lazzarino, G. and Di, Pietro V. and Tavazzi, B. and Belli, A. and Logan, A.}, doi = {10.3390/antiox9090850}, journal-iso = {ANTIOXIDANTS-BASEL}, journal = {ANTIOXIDANTS}, volume = {9}, unique-id = {31666292}, year = {2020}, eissn = {2076-3921} } @article{MTMT:31349689, title = {Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes From Children With DCMA, a Mitochondrial Cardiomyopathy}, url = {https://m2.mtmt.hu/api/publication/31349689}, author = {Rohani, Leili and Machiraju, Pranav and Sabouny, Rasha and Meng, Guoliang and Liu, Shiying and Zhao, Tian and Iqbal, Fatima and Wang, Xuemei and Ravandi, Amir and Wu, Joseph C. and Khan, Aneal and Shutt, Timothy and Rancourt, Derrick and Greenway, Steven C.}, doi = {10.1016/j.cjca.2019.09.021}, journal-iso = {CAN J CARDIOL}, journal = {CANADIAN JOURNAL OF CARDIOLOGY}, volume = {36}, unique-id = {31349689}, issn = {0828-282X}, year = {2020}, eissn = {1916-7075}, pages = {554-563}, orcid-numbers = {Sabouny, Rasha/0000-0001-8698-9291; Shutt, Timothy/0000-0001-5299-2943} } @article{MTMT:31349701, title = {Chronic imaging of mitochondria in the murine cerebral vasculature using in vivo two-photon microscopy}, url = {https://m2.mtmt.hu/api/publication/31349701}, author = {Rutkai, I. and Evans, W.R. and Bess, N. and Salter-Cid, T. and Cikic, S. and Chandra, P.K. and Katakam, P.V.G. and Mostany, R. and Busija, D.W.}, doi = {10.1152/ajpheart.00751.2019}, journal-iso = {AM J PHYSIOL HEART C}, journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY}, volume = {318}, unique-id = {31349701}, issn = {0363-6135}, year = {2020}, eissn = {1522-1539}, pages = {H1379-H1386} } @article{MTMT:31607817, title = {Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases}, url = {https://m2.mtmt.hu/api/publication/31607817}, author = {Song, K. and Li, Y. and Zhang, H. and An, N. and Wei, Y. and Wang, L. and Tian, C. and Yuan, M. and Sun, Y. and Xing, Y. and Gao, Y. and Santibañez, J.F.}, doi = {10.1155/2020/4356386}, journal-iso = {OXID MED CELL LONGEV}, journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY}, volume = {2020}, unique-id = {31607817}, issn = {1942-0900}, abstract = {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.}, keywords = {Brain; Brain; Inflammation; BLOOD; BLOOD; DAMAGE; SYSTEMS; MATRIX METALLOPROTEINASES; cytokine; Pathogenesis; review; neurologic disease; human; diabetes mellitus; HYPERTENSION; ANTIOXIDANT; nonhuman; brain ischemia; brain hemorrhage; IRON; biological marker; DISEASES; Production; cerebrovascular disease; reactive oxygen metabolite; traumatic brain injury; Parkinson's disease; neurodegenerative diseases; mitochondrial dysfunction; excitotoxicity; Parkinson disease; BARRIERS; neurology; neurology; heart infarction; Inflammatory response; disorders of mitochondrial functions; matrix metalloproteinase; Cell Death; Alzheimer disease; blood brain barrier; carrier protein; stresses; iron metabolism; intestine flora; tight junction; amyotrophic lateral sclerosis; amyotrophic lateral sclerosis; medical decision making; NEUROLOGICAL DISEASE; Necroptosis; Pyroptosis; traumatic brain injuries; myocardial ischemia reperfusion injury; autophagy (cellular); Oxidative stress; Oxidative stress; Molecular exchanges}, year = {2020}, eissn = {1942-0994} } @article{MTMT:32686573, title = {Analysis of factors affecting cognitive function in patients with traumatic brain injury}, url = {https://m2.mtmt.hu/api/publication/32686573}, author = {Zhang, Qi and Liu, Su and Sun, Li and Zhu, Zhenjie and Qin, Zhengji and Shen, Guangyu}, doi = {10.3760/cma.j.cn311847-20191209-00374}, journal = {Chinese Journal of Nautical Medicine and Hyperbaric Medicine}, volume = {27}, unique-id = {32686573}, issn = {1009-6906}, abstract = {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.}, keywords = {cognition; traumatic brain injury}, year = {2020}, pages = {427-432} }