@article{MTMT:34756766,
	title = {The Molecular Blueprint for Chronic Obstructive Pulmonary Disease (COPD): A New Paradigm for Diagnosis and Therapeutics},
	url = {https://m2.mtmt.hu/api/publication/34756766},
	author = {Shakeel, I. and Ashraf, A. and Afzal, M. and Sohal, S.S. and Islam, A. and Kazim, S.N. and Hassan, M.I.},
	doi = {10.1155/2023/2297559},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34756766},
	issn = {1942-0900},
	abstract = {The global prevalence of chronic obstructive pulmonary disease (COPD) has increased over the last decade and has emerged as the third leading cause of death worldwide. It is characterized by emphysema with prolonged airflow limitation. COPD patients are more susceptible to COVID-19 and increase the disease severity about four times. The most used drugs to treat it show numerous side effects, including immune suppression and infection. This review discusses a narrative opinion and critical review of COPD. We present different aspects of the disease, from cellular and inflammatory responses to cigarette smoking in COPD and signaling pathways. In addition, we highlighted various risk factors for developing COPD apart from smoking, like occupational exposure, pollutants, genetic factors, gender, etc. After the recent elucidation of the underlying inflammatory signaling pathways in COPD, new molecular targeted drug candidates for COPD are signal-transmitting substances. We further summarize recent developments in biomarker discovery for COPD and its implications for disease diagnosis. In addition, we discuss novel drug targets for COPD that could be explored for drug development and subsequent clinical management of cardiovascular disease and COVID-19, commonly associated with COPD. Our extensive analysis of COPD cause, etiology, diagnosis, and therapeutic will provide a better understanding of the disease and the development of effective therapeutic options. In-depth knowledge of the underlying mechanism will offer deeper insights into identifying novel molecular targets for developing potent therapeutics and biomarkers of disease diagnosis. © 2023 Ilma Shakeel et al.},
	keywords = {Humans; DRUGS; FIBRINOGEN; INFECTION; exposure; signal transduction; DEPRESSION; ANGIOGENESIS; review; review; human; diabetes mellitus; air pollution; Drug Interactions; Risk Factors; Biomarkers; risk factor; smoking; ANTIOXIDANT; nonhuman; diagnosis; diagnosis; Development; disease severity; Aging; gender; occupational exposure; DISEASES; Comorbidity; ANEMIA; MANAGEMENT; PROTEIN FUNCTION; heart failure; heredity; cardiovascular disease; Lung; Lung; interleukin 6; Tumor Necrosis Factor; side effect; pulmonary hypertension; coronary artery disease; osteoporosis; lung cancer; social status; cigarette smoking; C reactive protein; Inflammatory response; immunoglobulin enhancer binding protein; ADAPTIVE IMMUNITY; matrix metalloproteinase; HYPOXIA; IMMUNE SUPPRESSION; Complication; protein inhibitor; malnutrition; Pulmonary Disease, Chronic Obstructive; chronic obstructive lung disease; chronic obstructive lung disease; phosphodiesterase IV inhibitor; proteinase inhibitor; cell adhesion molecule; arterial stiffness; muscle disease; lung emphysema; chronic obstructive pulmonary disease; signalling pathways; Pulmonary diseases; Obstructive sleep apnea; serum amyloid A; Cellular response; peroxisome proliferator activated receptor agonist; PULMONARY EMPHYSEMA; Causes of death; DISEASE DIAGNOSIS; Critical review; COVID-19; COVID-19; coronavirus disease 2019; coronavirus disease 2019; COVID-19 Testing; COVID-19 Testing; NF kB signaling; Blueprints; normocytic anemia; Sides},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34399005,
	title = {Protective Potentials of Alpha-Lipoic Acid against Ionizing Radiation-Induced Brain Damage in Rats},
	url = {https://m2.mtmt.hu/api/publication/34399005},
	author = {Xu, J. and Alameri, A.A. and Zabibah, R.S. and Gabr, G.A. and Ramírez-Coronel, A.A. and Bagheri, H. and Abedi-Firouzjah, R.},
	doi = {10.1155/2023/4999306},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34399005},
	issn = {1942-0900},
	abstract = {Background. This study was aimed at determining the effects of alpha-lipoic acid on ionizing irradiation-induced oxidative damage and apoptosis in the brain of rats. Methods. The animals were exposed to whole-brain X-radiation with a 15 Gy single dose in the absence or presence of alpha-lipoic acid (200 mg/kg body weight) pretreatment for one week. The rats were divided into four groups (5 rats in each group): vehicle control, alpha-lipoic acid alone (ALA), radiation alone (RAD), and radiation plus alpha-lipoic acid (RAD+ALA). In the next stage, malondialdehyde (MDA), nitric oxide, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in the brain tissue of the rats were measured. Furthermore, the Western blot analysis technique was performed to assess the NOX2, NOX4, and caspase-3 protein expression levels. Results. Twenty-four hours after the irradiation, MDA and nitric oxide levels in the irradiated rats were significantly higher than those in the control group (p<0.001); however, the pretreatment with alpha-lipoic acid resulted in a significant reduction in these stress oxidative markers (p<0.05). Moreover, a significant decrease in CAT, SOD, and GPx levels was observed in the radiation group alone compared to the control group (p<0.01); in contrast, the activities of these antioxidant enzymes significantly increased in the radiation plus alpha-lipoic acid group in comparison to the radiation group alone (p<0.05). The results of Western blot analysis revealed that NOX2, NOX4, and caspase-3 protein expressions significantly elevated in the irradiated rats compared to the control group (p<0.001). The pretreatment with alpha-lipoic acid could significantly decrease the expression levels of NOX2, NOX4, and caspase-3 in comparison with the radiation group alone (p<0.05). Conclusion. According to the obtained findings, it can be mentioned that the alpha-lipoic acid pretreatment could mitigate the ionizing irradiation-induced oxidative damage and apoptosis in the brain of the rats. © 2023 Ji Xu et al.},
	keywords = {Brain; Brain; Animals; Body Weight; APOPTOSIS; metabolism; DAMAGE; RATS; RATS; ARTICLE; antioxidants; animal; OXIDATION; controlled study; ANTIOXIDANT; nonhuman; animal tissue; animal model; animal experiment; drug effect; IRRADIATION; enzyme activity; premedication; brain tissue; Western blotting; ELECTROPHORESIS; glutathione peroxidase; glutathione peroxidase; glutathione peroxidase; malondialdehyde; Catalase; Superoxide dismutase; Superoxide dismutase; Superoxide dismutase; malonaldehyde; brain damage; OXIDATIVE DAMAGE; PRETREATMENT; nitric oxide; nitric oxide; nitric oxide; nitric oxide; ACIDS; IONIZATION; radiation dose; X ray; Cell Death; Radiation Effects; ionizing radiation; ionizing radiation; ionizing radiation; Ionizing irradiation; Control systems; Control system synthesis; Caspase 3; Caspase 3; thioctic acid; thioctic acid; Caspase-3; Control Groups; Pre-treatments; Radiation, Ionizing; Superoxide dismutases; protein expression level; Bombax; Super oxide dismutase; rat; Oxidative stress; Oxidative stress; Decrements; Lipoic acids},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34395240,
	title = {Downregulation of Nrf2 in the Hippocampus Contributes to Postoperative Cognitive Dysfunction in Aged Rats by Sensitizing Oxidative Stress and Neuroinflammation},
	url = {https://m2.mtmt.hu/api/publication/34395240},
	author = {Li, L. and Meng, F. and Li, D.},
	doi = {10.1155/2023/7272456},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34395240},
	issn = {1942-0900},
	abstract = {Postoperative cognitive dysfunction (POCD) is a recognized clinical complication defined by a new cognitive impairment arising after a surgical procedure. Elderly patients are especially vulnerable to cognitive impairment after surgical operations, but the underlying mechanisms remain elusive. Oxidative stress and neuroinflammation in the hippocampus, a brain region involved in memory formation, are considered as major contributors to the development of POCD. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of endogenous inducible defense system, plays a crucial role in protecting cells against oxidative stress and inflammation by enhancing transcription of antioxidant and anti-inflammatory target genes. Here, we examined whether aging downregulates Nrf2 in the hippocampus and, if so, whether downregulation of hippocampal Nrf2 contributes to POCD in aging. Young and aged rats underwent abdominal surgery or sham operation. One week later, cognitive function was assessed, and brains were collected for molecular studies. Compared with young sham rats, aged sham rats exhibited a significant reduction in expression of Nrf2 in the hippocampus. Interestingly, the expression of Nrf2 downstream target genes and levels of reactive oxygen species (ROS) and proinflammatory cytokines in the hippocampus as well as cognitive function were comparable between aged sham and young sham rats. After abdominal surgery, young rats showed significant upregulation of Nrf2 and its target genes in the hippocampus. However, aged rats did not show changes in expression of Nrf2 and its target genes but had increased levels of ROS and proinflammatory cytokines in the hippocampus, along with cognitive impairment as indicated by reduced contextual freezing time. Moreover, upregulation of hippocampal Nrf2 in aged rats with intracerebroventricular infusion of a Nrf2 activator reduced levels of ROS and proinflammatory cytokines in the hippocampus, ameliorating cognitive dysfunction after surgery. The results suggest that aging-induced downregulation of Nrf2 in the hippocampus causes the failure to activate Nrf2-regulated antioxidant defense system in response to surgical insult, which contributes to POCD by sensitizing oxidative stress and neuroinflammation. Nrf2 activation in the brain may be a novel strategy to prevent the cognitive decline in elderly patients after surgery. © 2023 Liang Li et al.},
	keywords = {Brain; Animals; Aged; Adult; Male; CELLS; metabolism; ACTIVATION; GENES; SYSTEMS; TRANSCRIPTION; hippocampus; hippocampus; hippocampus; RATS; RATS; ARTICLE; antioxidants; antioxidants; antioxidants; Cytokines; cytokine; animal; Up-Regulation; physiology; controlled study; ANTIOXIDANT; nonhuman; animal model; animal experiment; light dark cycle; cognition; Aging; Western blotting; REDUCTION; Young Adult; Down-Regulation; Down-Regulation; surgery; hydrogen peroxide; protein expression; interleukin 6; messenger rna; Chemical activation; Reactive oxygen species; Reactive oxygen species; reactive oxygen metabolite; reactive oxygen metabolite; COGNITIVE FUNCTIONS; COGNITIVE DYSFUNCTION; laparotomy; COGNITIVE IMPAIRMENT; neuroinflammation; abdominal surgery; abdominal surgery; upregulation; interleukin 1beta; down regulation; down regulation; cognitive defect; cognitive defect; real time polymerase chain reaction; heme oxygenase 1; stresses; sham procedure; open field test; nervous system inflammation; manganese superoxide dismutase; beta actin; TARGET GENES; PROINFLAMMATORY CYTOKINES; transcription factor Nrf2; transcription factor Nrf2; Network security; Postoperative cognitive dysfunction; NF-E2-Related Factor 2; bardoxolone methyl; fear conditioning test; rat; clinical complications; number of rearings; number of crossings; Oxidative stress; Oxidative stress; Oxidative stress; Oxidative stress; neuroinflammatory diseases; postoperative cognitive complications},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34395199,
	title = {Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N -Acetylcysteine on Colon, Liver, and Kidney},
	url = {https://m2.mtmt.hu/api/publication/34395199},
	author = {Da, Paz Martins A.S. and De, Andrade K.Q. and De, Araújo O.R.P. and Da, Conceição G.C.M. and Da, Silva Gomes A. and Goulart, M.O.F. and Moura, F.A.},
	doi = {10.1155/2023/8811463},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34395199},
	issn = {1942-0900},
	abstract = {Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease (IBD) characterized by continuous inflammation in the colonic mucosa. Extraintestinal manifestations (EIM) occur due to the disruption of the intestinal barrier and increased permeability caused by redox imbalance, dysbiosis, and inflammation originating from the intestine and contribute to morbidity and mortality. The aim of this study is to investigate the effects of oral N-acetylcysteine (NAC) on colonic, hepatic, and renal tissues in mice with colitis induced by dextran sulfate sodium (DSS). Male Swiss mice received NAC (150 mg/kg/day) in the drinking water for 30 days before and during (DSS 5% v/v; for 7 days) colitis induction. On the 38th day, colon, liver, and kidney were collected and adequately prepared for the analysis of oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione reduced (GSH), glutathione oxidized (GSSG), malondialdehyde (MDA), and hydrogen peroxide (H2O2)) and inflammatory biomarkers (myeloperoxidase (MPO) -, tumor necrosis factor alpha - (TNF-α, and interleukin-10 (IL-10)). In colon, NAC protected the histological architecture. However, NAC did not level up SOD, in contrast, it increased MDA and pro-inflammatory effect (increased of TNF-α and decreased of IL-10). In liver, colitis caused both oxidative (MDA, SOD, and GSH) and inflammatory damage (IL-10). NAC was able only to increase GSH and GSH/GSSG ratio. Kidney was not affected by colitis; however, NAC despite increasing CAT, GSH, and GSH/GSSG ratio promoted lipid peroxidation (increased MDA) and pro-inflammatory action (decreased IL-10). Despite some beneficial antioxidant effects of NAC, the negative outcomes concerning irreversible oxidative and inflammatory damage in the colon, liver, and kidney confirm the nonsafety of the prophylactic use of this antioxidant in models of induced colitis, suggesting that additional studies are needed, and its use in humans not yet recommended for the therapeutic routine of this disease. © 2023 Amylly Sanuelly da Paz Martins et al.},
	keywords = {Animals; Adult; Male; Male; Inflammation; Inflammation; Humans; PEPTIDES; COLON; COLON; metabolism; LIVER; LIVER; MICE; DAMAGE; ARTICLE; ANTIINFLAMMATORY ACTIVITY; SODIUM; MOUSE; antioxidants; antioxidants; Tumor necrosis factor-alpha; Inflammatory bowel disease; human; animal; OXIDATION; SULFATES; SULFUR COMPOUNDS; Lipid Peroxidation; Plants (botany); ulcerative colitis; ulcerative colitis; Colitis, Ulcerative; controlled study; GLUTATHIONE; GLUTATHIONE; GLUTATHIONE; ANTIOXIDANT; GLUCOSE; nonhuman; glucose blood level; animal tissue; animal model; animal experiment; pathology; pathology; Histology; Permeability; DISEASES; malondialdehyde; hydrogen peroxide; hydrogen peroxide; hydrogen peroxide; hydrogen peroxide; interleukin 10; interleukin 10; Catalase; Tumor Necrosis Factor; Tumor Necrosis Factor; Interleukin-10; Interleukin-10; antioxidant activity; Superoxide dismutase; Superoxide dismutase; Superoxide dismutase; Superoxide dismutase; malonaldehyde; KETAMINE; myeloperoxidase; COLITIS; COLITIS; MAMMALS; drinking water; acetylcysteine; acetylcysteine; acetylcysteine; renal protection; dextran sulfate; dextran sulfate; Cell Death; Complication; Glutathione Disulfide; Glutathione Disulfide; Glutathione Disulfide; Potable water; N-acetylcysteine; stresses; liver protection; Liver tissue; INCREMENTS; Superoxide dismutases; Swiss Webster mouse; kidney tissue; redox stress; xylazine; Super oxide dismutase; Dextran sulfate sodium; colon tissue; Oxidative stress; Oxidative stress; Oxidative stress; dextran sulfate sodium-induced acute colitis; TNF α; Inflammatory damages},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34391822,
	title = {Traxoprodil Produces Antidepressant-Like Behaviors in Chronic Unpredictable Mild Stress Mice through BDNF/ERK/CREB and AKT/FOXO/Bim Signaling Pathway},
	url = {https://m2.mtmt.hu/api/publication/34391822},
	author = {Wang, Y. and Liang, Z. and Song, W. and Qin, Y. and Todd, N. and Gao, M.},
	doi = {10.1155/2023/1131422},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34391822},
	issn = {1942-0900},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34323362,
	title = {Empagliflozin-Pretreated Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Attenuated Heart Injury},
	url = {https://m2.mtmt.hu/api/publication/34323362},
	author = {Chi, B. and Zou, A. and Mao, L. and Cai, D. and Xiao, T. and Wang, Y. and Wang, Q. and Ji, Y. and Sun, L.},
	doi = {10.1155/2023/7747727},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34323362},
	issn = {1942-0900},
	abstract = {Objective. Small extracellular vesicles derived from mesenchymal stem cells (MSCs) play important roles in cardiac protection. Studies have shown that the cardiovascular protection of sodium-glucose cotransporter 2 inhibitor (SGLT2i) is independent of its hypoglycemic effect. This study is aimed at investigating whether small extracellular vesicles derived from MSCs pretreated with empagliflozin (EMPA) has a stronger cardioprotective function after myocardial infarction (MI) and to explore the underlying mechanisms. Methods and Results. We evaluated the effects of EMPA on MSCs and the effects of EMPA-pretreated MSCs-derived small extracellular vesicles (EMPA-sEV) on myocardial apoptosis, angiogenesis, and cardiac function after MI in vitro and in vivo. The small extracellular vesicles of control MSCs (MSC-sEV) and EMPA-pretreated MSCs were extracted, respectively. Small extracellular vesicles were cocultured with apoptotic H9c2 cells induced by H2O2 or injected into the infarcted area of the Sprague-Dawley (SD) rat myocardial infarction model. EMPA increased the cell viability, migration ability, and inhibited apoptosis and senescence of MSCs. In vitro, EMPA-sEV inhibited apoptosis of H9c2 cells compared with the control group (MSC-sEV). In the SD rat model of MI, EMPA-sEV inhibited myocardial apoptosis and promoted angiogenesis in the infarct marginal areas compared with the MSC-sEV. Meanwhile, EMPA-sEV reduced infarct size and improved cardiac function. Through small extracellular vesicles (miRNA) sequencing, we found several differentially expressed miRNAs, among which miR-214-3p was significantly elevated in EMPA-sEV. Coculture of miR-214-3p high expression MSC-derived small extracellular vesicles with H9c2 cells produced similar protective effects. In addition, miR-214-3p was found to promote AKT phosphorylation in H9c2 cells. Conclusions. Our data suggest that EMPA-sEV significantly improve cardiac repair after MI by inhibiting myocardial apoptosis. miR-214-3p at least partially mediated the myocardial protection of EMPA-sEV through the AKT signaling pathway. © 2023 Boyu Chi et al.},
	keywords = {Animals; Male; PHOSPHORYLATION; CELLS; APOPTOSIS; IN-VITRO; immunohistochemistry; RATS; RATS; ARTICLE; PROTECTION; SODIUM; RNA; ANGIOGENESIS; ANGIOGENESIS; Stem Cells; human; animal; Rats, Sprague-Dawley; Nucleic Acids; controlled study; HEART; GLUCOSE; nonhuman; animal model; animal experiment; animal cell; cell proliferation; MAINTENANCE; in vitro study; protein phosphorylation; Western blotting; hydrogen peroxide; hydrogen peroxide; human cell; cell culture; cell migration; particle size; heart function; in vivo study; myocardial infarction; myocardial infarction; heart infarction; heart infarction; enzyme phosphorylation; SPRAGUE-DAWLEY RATS; Cell viability; upregulation; Cardiology; Sprague Dawley rat; Cell Death; down regulation; heart protection; protein bcl 2; protein Bax; Control systems; real time polymerase chain reaction; senescence; Proto-Oncogene Proteins c-akt; Caspase 3; caspase 7; Mesenchymal Stem Cells; mesenchymal stem cell; mesenchymal stem cell; beta galactosidase; exosome; Extracellular; cardiac muscle; CD63 antigen; glyceraldehyde 3 phosphate dehydrogenase; Heart Injuries; heart injury; protein kinase B; protein kinase B; Flowcharting; Extracellular vesicles; Cardiac functions; Akt signaling; H9c2(2-1) cell line; CD81 antigen; tumor susceptibility gene 101 protein; Empagliflozin; Empagliflozin; rat; bone marrow mesenchymal stem cell; H9C2 cells; myocardial apoptosis; antiapoptosis; microRNA 214; Cardiovascular protections},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34315895,
	title = {Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials},
	url = {https://m2.mtmt.hu/api/publication/34315895},
	author = {Luan, Y. and Jiang, L. and Luan, Y. and Xie, Y. and Yang, Y. and Ren, K.-D.},
	doi = {10.1155/2023/1649842},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34315895},
	issn = {1942-0900},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34213476,
	title = {Photobiomodulation at Defined Wavelengths Regulates Mitochondrial Membrane Potential and Redox Balance in Skin Fibroblasts},
	url = {https://m2.mtmt.hu/api/publication/34213476},
	author = {Baldassarro, V.A. and Alastra, G. and Lorenzini, L. and Giardino, L. and Calzà, L.},
	doi = {10.1155/2023/7638223},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34213476},
	issn = {1942-0900},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34208517,
	title = {MicroRNAs Regulate Function in Atherosclerosis and Clinical Implications},
	url = {https://m2.mtmt.hu/api/publication/34208517},
	author = {Li, Z. and Zhao, Y. and Suguro, S. and Suguro, R.},
	doi = {10.1155/2023/2561509},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34208517},
	issn = {1942-0900},
	abstract = {Background. Atherosclerosis is considered the most common cause of morbidity and mortality worldwide. Athermanous plaque formation is pathognomonic of atherosclerosis. The main feature of atherosclerosis is the formation of plaque, which is inseparable from endothelial cells, vascular smooth muscle cells, and macrophages. MicroRNAs, a small highly conserved noncoding ribonucleic acid (RNA) molecule, have multiple biological functions, such as regulating gene transcription, silencing target gene expression, and affecting protein translation. MicroRNAs also have various pharmacological activities, such as regulating cell proliferation, apoptosis, and metabolic processes. It is noteworthy that many studies in recent years have also proved that microRNAs play a role in atherosclerosis. Methods. To summarize the functions of microRNAs in atherosclerosis, we reviewed all relevant articles published in the PubMed database before June 2022, with keywords "atherosclerosis,""microRNA,""endothelial cells,""vascular smooth muscle cells,""macrophages,"and "cholesterol homeostasis,"briefly summarized a series of research progress on the function of microRNAs in endothelial cells, vascular smooth muscle cells, and macrophages and atherosclerosis. Results and Conclusion. In general, the expression levels of some microRNAs changed significantly in different stages of atherosclerosis pathogenesis; therefore, MicroRNAs may become new diagnostic biomarkers for atherosclerosis. In addition, microRNAs are also involved in the regulation of core processes such as endothelial dysfunction, plaque formation and stabilization, and cholesterol metabolism, which also suggests the great potential of microRNAs as a therapeutic target. © 2023 Zhaoyi Li et al.},
	keywords = {Humans; CELLS; ATHEROSCLEROSIS; ATHEROSCLEROSIS; ENDOTHELIAL-CELLS; metabolism; metabolism; MACROPHAGES; GENETICS; MUSCLE; TRANSCRIPTION; RNA; human; cell proliferation; STABILIZATION; DISEASES; lipid metabolism; lipid metabolism; cholesterol; cholesterol; cholesterol; ACIDS; microRNA; endothelium cell; endothelial cells; endothelial cells; Cell Death; Control systems; MICRORNAS; biological functions; CORES; Metabolic process; vascular smooth muscle cells; Formation; Processes; Protein translation; Pharmacological activity; Target gene expression; Cholesterol homeostasis; Gene transcriptions; Acid molecules},
	year = {2023},
	eissn = {1942-0994}
}

@article{MTMT:34105123,
	title = {NAD+-Consuming Enzymes in Stem Cell Homeostasis},
	url = {https://m2.mtmt.hu/api/publication/34105123},
	author = {Ji, X. and Zheng, M. and Yu, T. and Kang, J. and Fan, T. and Xu, B.},
	doi = {10.1155/2023/4985726},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2023},
	unique-id = {34105123},
	issn = {1942-0900},
	abstract = {Nicotinamide adenine dinucleotide (NAD+) is a coenzyme used in redox reactions, energy metabolism, and mitochondrial biogenesis. NAD+ is also required as a cofactor by nonredox NAD+-dependent enzymes. Hundreds of enzymes that consume NAD+ have been identified. The NAD+-consuming enzymes are involved in a variety of cellular processes such as signal transduction, DNA repair, cellular senescence, and stem cell (SC) homeostasis. In this review, we discussed how different types of NAD+-consuming enzymes regulate SC functions and summarized current research on the roles of the NAD+ consumers in SC homeostasis. We hope to provide a more global and integrative insight to the mechanism and intervention of SC homeostasis via the regulation of the NAD+-consuming enzymes. © 2023 Xiuna Ji et al.},
	keywords = {metabolism; metabolism; metabolism; ENZYMES; signal transduction; signal transduction; signal transduction; Stem Cells; stem cell; review; human; Nucleic Acids; nonhuman; MAINTENANCE; Oxidation-Reduction; Homeostasis; Homeostasis; Homeostasis; PROTEIN FUNCTION; unclassified drug; research; energy metabolism; energy metabolism; energy metabolism; redox reactions; redox reactions; oxidation reduction reaction; sirtuin 1; DNA-REPAIR; MITOCHONDRIAL BIOGENESIS; Control systems; NAD; nicotinamide adenine dinucleotide; nicotinamide adenine dinucleotide; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase; Coenzymes; Reaction energy; cellular senescence; sirtuin 3; sirtuin 2; Consumers; STEM-CELL; sirtuin 4; sirtuin 5; sirtuin 6; sirtuin 7; ADP ribosyl cyclase/cyclic ADP ribose hydrolase 1; Cellular process; cofactors; CD157 antigen; Nicotinamide adenine dinucleotides; cell homeostasis; sterile alpha and toll interleukin receptor motif containing 1},
	year = {2023},
	eissn = {1942-0994}
}