Article
Biotechnology & Applied Microbiology
Xindong Liu, Xin Wang, Lijuan Zhang, Yi Zhou, Le Yang, Minghao Yang
Summary: This study investigated the role of miR-484 in regulating neuronal apoptosis induced by cerebral ischemia/reperfusion injury in mice. Upregulation of miR-484 was found to increase neuronal viability and inhibit apoptosis by targeting BCL2L13. These findings suggest that miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis by targeting the apoptosis facilitator BCL2L13.
Letter
Neurosciences
Shitao Lv, Haiyan Yang, Pengcheng Jing, Haiying Song
Summary: Alpha-tocopherol has shown antioxidant, anti-inflammatory, and anti-apoptotic abilities in rat brain tissue, mitigating nerve damage caused by cerebral ischemia-reperfusion injury.
CNS NEUROSCIENCE & THERAPEUTICS
(2022)
Article
Biochemistry & Molecular Biology
Yongbo Yu, Qian Xia, Gaofeng Zhan, Shuai Gao, Tangrui Han, Meng Mao, Xing Li, Yonghong Wang
Summary: This study identified the role of TRIM67 in ischemia.reperfusion injury, showing that upregulation of TRIM67 can regulate neuroinflammation and neuronal apoptosis, providing therapeutic benefits for ischemic stroke.
CELL AND BIOSCIENCE
(2023)
Article
Biochemistry & Molecular Biology
Zhe Liu, Guangze Mou, Zhiming Liang, Rui Zhao, Chenghao Jin, Rui Wu
Summary: The study found that selenomethionine (SeMet) can alleviate intestinal ischemia-reperfusion injury by increasing antioxidant levels and inhibiting the expression of apoptosis-related proteins.
BIOLOGICAL TRACE ELEMENT RESEARCH
(2022)
Article
Chemistry, Medicinal
Jiangbo Xie, Tingting Zhang, Peichun Li, Dong Wang, Tao Liu, Shunliang Xu
Summary: This study found that dihydromyricetin can alleviate cerebral ischemia reperfusion injury by inhibiting the SPHK1/mTOR signaling pathway and suppressing ferroptosis. These findings suggest that dihydromyricetin may be a potential drug for the treatment of cerebral ischemia reperfusion injury.
DRUG DESIGN DEVELOPMENT AND THERAPY
(2022)
Article
Neurosciences
Yanan Li, Qianni Shen, Lidan Huang, Bingyu Li, Yuxi Zhang, Wei Wang, Bo Zhao, Wenwei Gao
Summary: This study investigates the role of GRSF1 in cerebral ischemia-reperfusion injury (CIRI) and its specific mechanisms. The researchers found that GRSF1 expression was low in CIR mice, while senescence-related markers were increased. Overexpression of GRSF1 improved infarct volume and neurological function, and suppressed apoptosis. The results suggest that cellular senescence contributes to CIRI, and GRSF1 can protect against reperfusion injury by regulating GPX4.
MOLECULAR NEUROBIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Mathias Clarysse, Alison Accarie, Arnau Panisello-Rosello, Ricard Farre, Emilio Canovai, Diethard Monbaliu, Gert De Hertogh, Tim Vanuytsel, Jacques Pirenne, Laurens J. Ceulemans
Summary: Intestinal ischemia-reperfusion injury (IRI) is a common clinical condition with unpredictable outcomes. Polyethylene glycol (PEG), a commonly used excipient, has been found to have anti-inflammatory and cell-membrane-stabilizing properties. This study investigated the effects of PEG administration on IRI in rats and found that it reduced reperfusion edema, bacterial translocation, inflammatory reaction, and improved survival.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Immunology
Kongwei Guo, Yanxing Shang, Zhao Wang, Yu Li, Jinliang Chen, Baofeng Zhu, Dongmei Zhang, Jianrong Chen
Summary: BRG1 plays a key role in apoptosis and oxidative damage, but its role in the pathophysiology of ischemic stroke is unclear. We found that BRG1 expression was increased during cerebral ischemia and reperfusion, particularly in activated microglia. Modulating BRG1 expression levels significantly affected microglial activation and the expression of antioxidant and pro-oxidant proteins after ischemic stroke. Our findings suggest that BRG1 protects against brain ischemia/reperfusion injury by reducing oxidative damage through the KEAP1-NRF2/HO-1 signaling pathway.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Pharmacology & Pharmacy
Zexuan Hong, Jun Cao, Dandan Liu, Maozhu Liu, Mengyuan Chen, Fanning Zeng, Zaisheng Qin, Jigang Wang, Tao Tao
Summary: Stroke is a major cause of death, with oxidative stress playing a key role. Celastrol has strong antioxidant properties, but its effect on oxidative reactions in cerebral ischemic-reperfusion injury (CIRI) is unclear. This study aimed to investigate the impact of celastrol on oxidative damage during CIRI and the underlying mechanisms. The findings revealed that celastrol reduced oxidative injury in CIRI by upregulating Nrf2. Celastrol directly bound to Nedd4, releasing Nrf2 in astrocytes, thus inhibiting Nrf2 degradation and reducing astrocytic ROS production. Celastrol also rescued neurons from damage and apoptosis by inhibiting oxidative stress and astrocyte activation.
JOURNAL OF PHARMACEUTICAL ANALYSIS
(2023)
Article
Cell Biology
Binbin Fang, Fen Liu, Xiaolin Yu, Junyi Luo, Xuehe Zhang, Tong Zhang, Jixin Zhang, Yining Yang, Xiaomei Li
Summary: Diabetic patients are prone to acute myocardial infarction, but liraglutide can reduce myocardial injury and improve cardiac function. This study shows that liraglutide exerts its protective effects through activation of AMPK/mTOR-mediated autophagy.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2023)
Article
Biotechnology & Applied Microbiology
Daozhou Liu, Qifeng Ji, Ying Cheng, Miao Liu, Bangle Zhang, Qibing Mei, Menglei Huan, Siyuan Zhou
Summary: CsA@HFn nanoparticles have shown significant therapeutic effects in the treatment of cerebral ischemia/reperfusion injury by alleviating neuron apoptosis, nerve inflammation, and blood-brain barrier damage in the ischemic area. CsA@HFn has great potential in the treatment of ischemic stroke.
JOURNAL OF NANOBIOTECHNOLOGY
(2022)
Article
Cell Biology
Rongchuan Yue, Shengzhong Lu, Yu Luo, Jing Zeng, Hao Liang, Dan Qin, Xiaobo Wang, Tao Wang, Jun Pu, Houxiang Hu
Summary: Recent evidence suggests that exosomal miR-182-5p derived from mesenchymal stem cells (MSCs) can protect against myocardial ischemia/reperfusion (I/R) injury by inhibiting GSDMD expression and reducing cell pyroptosis and inflammation. Moreover, MSC-derived exosomes carrying miR-182-5p can improve cardiac function and reduce myocardial infarction in vivo.
CELL DEATH DISCOVERY
(2022)
Article
Pharmacology & Pharmacy
Manisha Kawadkar, Avinash S. Mandloi, Vidhu Saxena, Chetana Tamadaddi, Chandan Sahi, Vipin V. Dhote
Summary: The study demonstrates the protective effect of noscapine in yeast and I-R rats by improving cell viability and attenuating neuronal damage, respectively. This protective activity of noscapine could be attributed to potent free radical scavenging and inhibition of inflammation in cerebral ischemia-reperfusion injury.
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
(2021)
Article
Immunology
Yanbin Song, Yunqing Zhang, Zhaofei Wan, Junqiang Pan, Feng Gao, Fei Li, Jing Zhou, Junmin Chen
Summary: In this study, the researchers found that CTRP3 was downregulated in patients with acute coronary syndrome (ACS) and mice with myocardial ischemia reperfusion (I/R) injury. Overexpression of CTRP3 improved cardiac function and attenuated myocardial injury caused by I/R. The protective effects of CTRP3 were mediated through the activation of the LAMP1/JIP2/JNK pathway, resulting in improved left ventricular function, decreased myocardial infarction, and reduced myocardial apoptosis.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Plant Sciences
Ping Huang, Si-Peng Wu, Ning Wang, Saiwang Seto, Dennis Chang
Summary: This study evaluated the protective effects of HSYA on cerebral I/R injury by inhibiting the opening of mPTP through the MEK/ERK/CypD pathway, reducing the release of CytC from mitochondria to protect cells and alleviate damage.
Article
Multidisciplinary Sciences
Irene Lopez-Fabuel, Marina Garcia-Macia, Costantina Buondelmonte, Olga Burmistrova, Nicolo Bonora, Paula Alonso-Batan, Brenda Morant-Ferrando, Carlos Vicente-Gutierrez, Daniel Jimenez-Blasco, Ruben Quintana-Cabrera, Emilio Fernandez, Jordi Llop, Pedro Ramos-Cabrer, Aseel Sharaireh, Marta Guevara-Ferrer, Lorna Fitzpatrick, Christopher D. Thompton, Tristan R. McKay, Stephan Storch, Diego L. Medina, Sara E. Mole, Peter O. Fedichev, Angeles Almeida, Juan P. Bolanos
Summary: The study reveals that failure in autophagy leads to the accumulation of impaired neuronal mitochondria in a CLN7 disease mouse model. It also shows that the increased activity of glycolytic enzyme PFKFB3 may contribute to the pathogenesis of CLN7 and that its inhibition can alleviate disease hallmarks.
NATURE COMMUNICATIONS
(2022)
Article
Pharmacology & Pharmacy
Rebeca Lapresa, Jesus Agulla, Sonia Gonzalez-Guerrero, Juan P. Bolanos, Angeles Almeida
Summary: This study found that oligomers of the amyloidogenic fragment 25-35 of the A beta peptide trigger Rock2 accumulation and activation. The activation of Rock2 is caused by the inactivation of Cdh1 through the Cdk5-Cdh1 signaling pathway. Inhibition of Rock2 activity rescues neuronal apoptosis and memory impairment caused by A beta 25-35 administration. This mechanism may contribute to neurodegeneration and memory loss in Alzheimer's disease.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Geriatrics & Gerontology
Moureq Alotaibi, Faten Al-Aqil, Faleh Alqahtani, Miteb Alanazi, Ahmed Nadeem, Sheikh F. Ahmad, Rebeca Lapresa, Metab Alharbi, Abdulrahman Alshammari, Muteb Alotaibi, Tareq Saleh, Raed Alrowis
Summary: This study investigated the neuroprotective effect of rapamycin in mitigating cisplatin-induced neurotoxicity. The results showed that rapamycin significantly reduced cisplatin-induced nociceptive-like symptoms and decreased the expression of inflammatory mediators. Additionally, rapamycin decreased neuronal apoptosis and reversed changes in protein expression associated with neurotoxicity. These findings suggest that rapamycin may be further investigated for the treatment of cisplatin-induced peripheral neuropathy.
FRONTIERS IN AGING NEUROSCIENCE
(2022)
Article
Biochemistry & Molecular Biology
Joao Victor Cabral-Costa, Carlos Vicente-Gutierrez, Jesus Agulla, Rebeca Lapresa, John W. Elrod, Angeles Almeida, Juan P. Bolanos, Alicia J. Kowaltowski
Summary: Intracellular Ca2+ concentrations are regulated by plasma membrane transporters, endoplasmic reticulum, and mitochondria. The mitochondrial calcium uniporter complex (MCUc) mediates Ca2+ uptake, while the mitochondrial Na+/Ca2+ exchanger (NCLX) facilitates Ca2+ efflux. The Nclx transcript is highly expressed in astrocytes compared to neurons. Inhibiting NCLX in mouse primary culture astrocytes resulted in altered Ca2+ signaling and increased glycolytic flux. Genetic deletion of NCLX in hippocampal astrocytes improved cognitive performance, while deletion in hippocampal neurons impaired cognition.
JOURNAL OF NEUROCHEMISTRY
(2023)
Review
Pharmacology & Pharmacy
Rebeca Lapresa, Jesus Agulla, Juan P. Bolanos, Angeles Almeida
Summary: Alzheimer's disease is the main cause of dementia in the elderly and there are currently no effective treatment options. Synapse dysfunction and loss are early pathological features, and inactivation of the APC/C enzyme leads to neurodegeneration and cognitive decline. Phosphorylation reactions induced by Alzheimer's disease exacerbate the enzyme inactivation, leading to the accumulation of multiple targets in damaged areas, further impairing neurons.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Angeles Almeida, Daniel Jimenez-Blasco, Juan P. Bolanos
Summary: This article focuses on the molecular mechanisms of energy and redox metabolism between astrocytes and neurons, to promote their coordinated functioning. Neurons have weaker basal glycolysis, promoting glucose-6-phosphate oxidation for antioxidant protection, while astrocytes have higher glycolytic activity and produce lactate as an oxidizable substrate for neurons. Additionally, neurons have more efficient mitochondrial respiratory chains with lower levels of reactive oxygen species (mROS), while astrocytes have higher mROS levels, which determine their specific transcriptional response and contribution to cognitive performance.
ESSAYS IN BIOCHEMISTRY
(2023)
Article
Multidisciplinary Sciences
Ana Paredes, Raquel Justo-Mendez, Daniel Jimenez-Blasco, Vanessa Nunez, Irene Calero, Maria Villalba-Orero, Andrea Alegre-Marti, Thierry Fischer, Ana Gradillas, Viviane Aparecida Rodrigues Sant'Anna, Felipe Were, Zhiqiang Huang, Pablo Hernansanz-Agustin, Carmen Contreras, Fernando Martinez, Emilio Camafeita, Jesus Vazquez, Jesus Ruiz-Cabello, Estela Area-Gomez, Fatima Sanchez-Cabo, Eckardt Treuter, Juan Pedro Bolanos, Eva Estebanez-Perpina, Francisco Javier Ruperez, Coral Barbas, Jose Antonio Enriquez, Mercedes Ricote
Summary: Birth poses a metabolic challenge to cardiomyocytes, requiring a transition from glucose to fatty acids as the main source of energy production. This transition is regulated by a fatty acid called ?-linolenic acid (GLA), present in maternal milk, which activates retinoid X receptors (RXRs) in embryonic cardiomyocytes. The lack of RXR leads to defective gene expression and abnormal mitochondrial fatty acid homeostasis, resulting in cardiac dysfunction and perinatal death. Supplementation of GLA induces RXR-dependent expression of mitochondrial fatty acid homeostasis genes in cardiomyocytes, both in vitro and in vivo.
Review
Biochemical Research Methods
Susana Campuzano, Rodrigo Barderas, Maria Teresa Moreno-Casbas, Angeles Almeida, Jose M. Pingarron
Summary: In the era of personalization, personalized management of medicine and nutrition is crucial for life expectancy and quality of life. Implementing precision medicine and nutrition is a complex challenge that requires new technologies to meet cost, simplicity, and versatility requirements, as well as accurately determining molecular markers in biofluids at different omics levels almost in real time. This review critically discusses recent advances and positions electrochemical bioplatforms as suitable tools for advanced diagnostics, therapy, and precision nutrition.
ANALYTICAL AND BIOANALYTICAL CHEMISTRY
(2023)
Article
Neurosciences
Daniel Jimenez-Blasco, Angeles Almeida, Juan P. Bolanos
Summary: This mini-review focuses on the contradiction between the high abundance of mitochondrial reactive oxygen species (mROS) in astrocytes and their essential role in cell metabolism and animal behavior. It discusses the mechanisms underlying the higher production of mROS in astrocytes compared to neurons, the specific molecular targets of astrocytic beneficial mROS, and the consequences of decreased astrocytic mROS leading to excess neuronal mROS and cellular damage. It aims to clarify the controversy surrounding the beneficial versus deleterious effects of ROS in the brain.
NEUROBIOLOGY OF DISEASE
(2023)
Article
Endocrinology & Metabolism
Brenda Morant-Ferrando, Daniel Jimenez-Blasco, Paula Alonso-Batan, Jesus Agulla, Rebeca Lapresa, Dario Garcia-Rodriguez, Sara Yunta-Sanchez, Irene Lopez-Fabuel, Emilio Fernandez, Peter Carmeliet, Angeles Almeida, Marina Garcia-Macia, Juan P. P. Bolanos
Summary: Astrocytes, a type of glial cells in the brain, primarily rely on glycolysis for energy production, indicating glucose as their main metabolic precursor. However, recent studies have shown that astrocytes also have the ability to metabolize fatty acids, and this metabolic pathway may play a role in preserving mitochondrial function and cognitive performance.