TY - JOUR AU - Shakeel, I. AU - Ashraf, A. AU - Afzal, M. AU - Sohal, S.S. AU - Islam, A. AU - Kazim, S.N. AU - Hassan, M.I. TI - The Molecular Blueprint for Chronic Obstructive Pulmonary Disease (COPD): A New Paradigm for Diagnosis and Therapeutics JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/2297559 UR - https://m2.mtmt.hu/api/publication/34756766 ID - 34756766 N1 - Department of Zoology, Aligarh Muslim University, Uttar Pradesh, Aligarh, 202002, India Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, New Delhi, 110025, India Respiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, College of Health and Medicine, University of Tasmania, Launceston, TAS 7248, Australia Export Date: 26 March 2024 Correspondence Address: Hassan, M.I.; Centre for Interdisciplinary Research in Basic Sciences, Jamia Nagar, India; email: mihassan@jmi.ac.in Chemicals/CAS: C reactive protein, 9007-41-4; fibrinogen, 9001-32-5; proteinase inhibitor, 37205-61-1 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Xu, J. AU - Alameri, A.A. AU - Zabibah, R.S. AU - Gabr, G.A. AU - Ramírez-Coronel, A.A. AU - Bagheri, H. AU - Abedi-Firouzjah, R. TI - Protective Potentials of Alpha-Lipoic Acid against Ionizing Radiation-Induced Brain Damage in Rats JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/4999306 UR - https://m2.mtmt.hu/api/publication/34399005 ID - 34399005 N1 - Department of Rehabilitation Medicine, 3201 Hospital, Hanzhong, 723000, China University of Babylon, Babylon, Iraq Medical Laboratory Technology Department, College of Medical Technology, Islamic University, Najaf, Iraq Department of Pharmacology and Toxicology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, 11942, Saudi Arabia Agricultural Genetic Engineering Research Institute (AGERI), Agricultural Research Center, Giza, Egypt Azogues Campus Nursing Career, Health and Behavior Research Group (HBR), Psychometry and Ethology Laboratory, Catholic University of Cuenca, Ecuador Doctorate in Psychology, University of Palermo, Buenos Aires, Argentina Epidemiology and Biostatistics Research Group, CES University, Colombia Radiation Sciences Research Center (RSRC), AJA University of Medical Sciences, Tehran, Iran Radiation Biology Research Center, Iran University of Medical Sciences, Tehran, Iran Department of Medical Physics Radiobiology and Radiation Protection, School of Medicine, Babol University of Medical Sciences, Babol, Iran Export Date: 25 November 2023 Correspondence Address: Bagheri, H.; Radiation Sciences Research Center (RSRC), Iran; email: hamed_parto@yahoo.com Correspondence Address: Abedi-Firouzjah, R.; Department of Medical Physics Radiobiology and Radiation Protection, Iran; email: razzaghabedi@gmail.com Chemicals/CAS: caspase 3, 169592-56-7; catalase, 9001-05-2; glutathione peroxidase, 9013-66-5; malonaldehyde, 542-78-9; nitric oxide, 10102-43-9; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; thioctic acid, 1077-29-8, 2319-84-8, 62-46-4; Antioxidants; Caspase 3; Glutathione Peroxidase; Nitric Oxide; Superoxide Dismutase; Thioctic Acid AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Li, L. AU - Meng, F. AU - Li, D. TI - Downregulation of Nrf2 in the Hippocampus Contributes to Postoperative Cognitive Dysfunction in Aged Rats by Sensitizing Oxidative Stress and Neuroinflammation JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/7272456 UR - https://m2.mtmt.hu/api/publication/34395240 ID - 34395240 N1 - Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, China Department of Anesthesiology, Jinan Maternity and Childcare Hospital, Jinan, China Cited By :3 Export Date: 22 November 2023 Correspondence Address: Li, D.; Department of Anesthesiology, China; email: ldl@sdu.edu.cn Chemicals/CAS: bardoxolone methyl, 218600-53-4; hydrogen peroxide, 7722-84-1; Antioxidants; Cytokines; NF-E2-Related Factor 2; Reactive Oxygen Species AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Da, Paz Martins A.S. AU - De, Andrade K.Q. AU - De, Araújo O.R.P. AU - Da, Conceição G.C.M. AU - Da, Silva Gomes A. AU - Goulart, M.O.F. AU - Moura, F.A. TI - Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N -Acetylcysteine on Colon, Liver, and Kidney JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/8811463 UR - https://m2.mtmt.hu/api/publication/34395199 ID - 34395199 N1 - Doctoral Program of the Northeast Biotechnology Network, Federal University of Alagoas, Alagoas, Maceió, 57072-970, Brazil College of Nutrition, Federal University of Alagoas, Alagoas, Maceió, 57072-970, Brazil Institute of Chemistry and Biotechnology, Federal University of Alagoas, Alagoas, Maceió, 57072-970, Brazil Institute of Biological and Health Sciences, Federal University of Alagoas, Alagoas, Maceió, 57072-970, Brazil College of Medicine, Federal University of Alagoas, Alagoas, Maceió, 57072-970, Brazil Export Date: 22 November 2023 Correspondence Address: Moura, F.A.; College of Nutrition, Alagoas, Brazil; email: fabiana.moura@fanut.ufal.br Chemicals/CAS: acetylcysteine, 616-91-1; catalase, 9001-05-2; glucose, 50-99-7, 84778-64-3, 8027-56-3; glutathione, 70-18-8; glutathione disulfide, 27025-41-8; hydrogen peroxide, 7722-84-1; ketamine, 1867-66-9, 6740-88-1, 81771-21-3; malonaldehyde, 542-78-9; myeloperoxidase; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xylazine, 23076-35-9, 7361-61-7; dextran sulfate, 9011-18-1, 9042-14-2; Acetylcysteine; Antioxidants; Dextran Sulfate; Glutathione; Glutathione Disulfide; Hydrogen Peroxide; Interleukin-10; Superoxide Dismutase; Tumor Necrosis Factor-alpha AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Wang, Y. AU - Liang, Z. AU - Song, W. AU - Qin, Y. AU - Todd, N. AU - Gao, M. TI - Traxoprodil Produces Antidepressant-Like Behaviors in Chronic Unpredictable Mild Stress Mice through BDNF/ERK/CREB and AKT/FOXO/Bim Signaling Pathway JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/1131422 UR - https://m2.mtmt.hu/api/publication/34391822 ID - 34391822 N1 - School of Pharmacy, China Medical University, Shenyang, 110122, China School of Medicine, Indiana University, Fort Wayne, 46805, United States Cited By :4 Export Date: 21 November 2023 Correspondence Address: Gao, M.; School of Pharmacy, China; email: mqgao26@cmu.edu.cn LA - English DB - MTMT ER - TY - JOUR AU - Chi, B. AU - Zou, A. AU - Mao, L. AU - Cai, D. AU - Xiao, T. AU - Wang, Y. AU - Wang, Q. AU - Ji, Y. AU - Sun, L. TI - Empagliflozin-Pretreated Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Attenuated Heart Injury JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/7747727 UR - https://m2.mtmt.hu/api/publication/34323362 ID - 34323362 N1 - Department of Cardiology, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Jiangsu, Changzhou, 213003, China Dalian Medical University, Liaoning, Dalian, 116000, China Cited By :1 Export Date: 14 November 2023 Correspondence Address: Wang, Q.; Department of Cardiology, Jiangsu, China; email: wang-qingjie@hotmail.com Correspondence Address: Ji, Y.; Department of Cardiology, Jiangsu, China; email: jiyuan1213@aliyun.com Correspondence Address: Sun, L.; Department of Cardiology, Jiangsu, China; email: sunling85125@hotmail.com Chemicals/CAS: beta galactosidase; caspase 3, 169592-56-7; caspase 7, 189258-14-8; empagliflozin, 864070-44-0; glyceraldehyde 3 phosphate dehydrogenase, 9001-50-7; protein bcl 2, 219306-68-0; protein kinase B, 148640-14-6; hydrogen peroxide, 7722-84-1; empagliflozin; Hydrogen Peroxide; Proto-Oncogene Proteins c-akt AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Luan, Y. AU - Jiang, L. AU - Luan, Y. AU - Xie, Y. AU - Yang, Y. AU - Ren, K.-D. TI - Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/1649842 UR - https://m2.mtmt.hu/api/publication/34315895 ID - 34315895 N1 - Cited By :1 Export Date: 1 February 2024 Correspondence Address: Yang, Y.; Clinical Systems Biology Research Laboratories, China; email: yangyangbio@163.com Correspondence Address: Xie, Y.; Department of Neurology, China; email: xysjkx@163.com Correspondence Address: Ren, K.-D.; Department of Pharmacy, China; email: renkd006@163.com LA - English DB - MTMT ER - TY - JOUR AU - Baldassarro, V.A. AU - Alastra, G. AU - Lorenzini, L. AU - Giardino, L. AU - Calzà, L. TI - Photobiomodulation at Defined Wavelengths Regulates Mitochondrial Membrane Potential and Redox Balance in Skin Fibroblasts JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/7638223 UR - https://m2.mtmt.hu/api/publication/34213476 ID - 34213476 N1 - Department of Veterinary Medical Sciences, University of Bologna, Via Tolara di Sopra 50, Ozzano dell'Emilia, Bologna, 40064, Italy Interdepartmental Centre for Industrial Research in Health Sciences and Technologies, University of Bologna, Via Tolara di Sopra 41/E, Ozzano dell'Emilia, Bologna, 40064, Italy Department of Pharmacy and Biotechnology, University of Bologna, Via Belmeloro 6, Bologna, 40126, Italy IRET Fundation, Via Tolara di Sopra 41/E, Ozzano dell'Emilia, Bologna, 40064, Italy Export Date: 24 October 2023 Correspondence Address: Calzà, L.; Interdepartmental Centre for Industrial Research in Health Sciences and Technologies, Via Tolara di Sopra 41/E, Ozzano dell'Emilia, Italy; email: laura.calza@unibo.it LA - English DB - MTMT ER - TY - JOUR AU - Li, Z. AU - Zhao, Y. AU - Suguro, S. AU - Suguro, R. TI - MicroRNAs Regulate Function in Atherosclerosis and Clinical Implications JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/2561509 UR - https://m2.mtmt.hu/api/publication/34208517 ID - 34208517 N1 - State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau Faculty of Medicine, School of Pharmacy, The Chinese University of Hong Kong, Shatin New Territories, Hong Kong, Hong Kong Export Date: 20 October 2023 Correspondence Address: Suguro, R.; State Key Laboratory of Quality Research in Chinese Medicine, Avenida Wai Long, Macau; email: rsuguro@must.edu.mo Chemicals/CAS: cholesterol, 57-88-5; Cholesterol; MicroRNAs AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Ji, X. AU - Zheng, M. AU - Yu, T. AU - Kang, J. AU - Fan, T. AU - Xu, B. TI - NAD+-Consuming Enzymes in Stem Cell Homeostasis JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2023 PY - 2023 SN - 1942-0900 DO - 10.1155/2023/4985726 UR - https://m2.mtmt.hu/api/publication/34105123 ID - 34105123 N1 - College of Marine Life Sciences, Ocean University of China, Qingdao, China Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China Affiliated Hospital of Qingdao University, Qingdao, China Export Date: 21 August 2023 Correspondence Address: Xu, B.; College of Marine Life Sciences, China; email: bxu@ouc.edu.cn Chemicals/CAS: nicotinamide adenine dinucleotide, 53-84-9; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase, 58319-92-9; NAD Funding details: National Natural Science Foundation of China, NSFC, 31601104 Funding details: Natural Science Foundation of Shandong Province, ZR2021MC158 Funding text 1: This work was supported by the National Natural Science Foundation of China (No. 31601104) and the Natural Science Foundation of Shandong Province (No. ZR2021MC158). AB - 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. LA - English DB - MTMT ER -