Journal of Bioenergetics and Biomembranes最新文献

{"title":"Hypoglycemic and hypolipidemic effect of pentaamino acid fullerene C₆₀ derivative in rats with metabolic disorder.","authors":"Yuliya V Soldatova,&nbsp;David A Areshidze,&nbsp;Maria A Kozlova,&nbsp;Alexander V Zhilenkov,&nbsp;Olga A Kraevaya,&nbsp;Irina I Faingold,&nbsp;Pavel A Troshin,&nbsp;Raisa A Kotelnikova","doi":"10.1007/s10863-023-09961-y","DOIUrl":"https://doi.org/10.1007/s10863-023-09961-y","url":null,"abstract":"<p><p>Pentaamino acid fullerene C₆₀ derivative is a promising nanomaterial, which exhibited antihyperglycemic activity in high-fat diet and streptozotocin-induced diabetic rats. This study investigates the effect of pentaaminoacid C₆₀ derivative (PFD) in rats with metabolic disorders. Rats were assigned to 3 groups (of 10 rats each) as follows: Group 1 (normal control), group 2 included the protamine-sulfate-treated rats (the untreated group of animals with the model metabolic disorder); group 3 (Protamine sulfate + PFD) included the protamine-sulfate-treated model rats that received an intraperitoneal injection of PFD. Metabolic disorder in rats was initiated by protamine sulfate (PS) administration. The PS + PFD group was injected intraperitoneally with PFD solution (3 mg/kg). Protamine sulfate induces biochemical changes (hyperglycemia, hypercholesterolemia, and hypertriglyceridemia) in the blood and morphological lesions in rat liver and pancreas. The potassium salt of fullerenylpenta-N-dihydroxytyrosine in protamine sulfate-induced rats normalized blood glucose level and the serum lipid profile and improved hepatic function markers. Treatment with PFD restored pancreas islets and liver structure of protamine sulfate-induced rats compared to the untreated group. PFD is a promising compound for further study as a drug against metabolic disorders.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 2","pages":"93-101"},"PeriodicalIF":3.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9550577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoenolpyruvate induces endothelial dysfunction and cell senescence through stimulation of metabolic reprogramming.","authors":"Tong An,&nbsp;Xiaoyi Zhang,&nbsp;Xin Gao,&nbsp;Xiyue Zhang,&nbsp;Tao Shen,&nbsp;Hongxia Li,&nbsp;Lin Dou,&nbsp;Xiuqing Huang,&nbsp;Yong Man,&nbsp;Guoping Li,&nbsp;Weiqing Tang,&nbsp;Jian Li","doi":"10.1007/s10863-023-09965-8","DOIUrl":"https://doi.org/10.1007/s10863-023-09965-8","url":null,"abstract":"<p><p>Endothelial dysfunction is a key early link in the pathogenesis of atherosclerosis, and the accumulation of senescent vascular endothelial cells causes endothelial dysfunction. Phosphoenolpyruvate (PEP), which is a high-energy glycolytic intermediate, protects against ischemia-reperfusion injury in isolated rat lung, heart, and liver tissue by quickly providing ATP. However, it was reported that serum PEP concentrations are 13-fold higher in healthy elderly compare to the young. Unlike that of other cell types, the energy required for the physiological function of endothelial cells is mainly derived from glycolysis. Recently, it is unclear whether circulating accumulation of PEP affects endothelial cell function. In this study, we found for the first time that 50-250 μM of PEP significantly promoted THP-1 monocyte adhesion to human umbilical vein endothelial cells (HUVECs) through increased expression of vascular endothelial adhesion factor 1 (VCAM1) and intercellular adhesion factor 1 (ICAM1) in HUVECs. Meanwhile, 50-250 μM of PEP decreased the expression of endothelial nitric oxide synthase (eNOS) and cellular level of nitric oxide (NO) in HUVECs. Moreover, PEP increased levels of ROS, enhanced the numbers of SA-β-Gal-positive cells and upregulated the expression of cell cycle inhibitors such as p21, p16 and the phosphorylation level of p53 on Ser15, and the expression of proinflammatory factors including TNF-α, IL-1β, IL-6, IL-8, IL-18 and MCP-1 in HUVECs. Furthermore, PEP increased both oxygen consumption rate (OCR) and glycolysis rate, and was accompanied by reduced NAD⁺/NADH ratios and enhanced phosphorylation levels of AMPKα (Thr172), p38 MAPK (T180/Y182) and NF-κB p65 (Ser536) in HUVECs. Notably, PEP had no significant effect on hepG2 cells. In conclusion, these results demonstrated that PEP induced dysfunction and senescence in vascular endothelial cells through stimulation of metabolic reprogramming.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 2","pages":"103-114"},"PeriodicalIF":3.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9551061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shrimp Glucose-6-phosphatase 2 (G6Pase 2): a second isoform of G6Pase in the Pacific white shrimp and regulation of G6Pase 1 and 2 isoforms via HIF-1 during hypoxia and reoxygenation in juveniles.","authors":"Laura E Hernández-Aguirre,&nbsp;Alma B Peregrino-Uriarte,&nbsp;Jorge L Duarte-Gutiérrez,&nbsp;Lilia Leyva-Carrillo,&nbsp;Josafat M Ezquerra-Brauer,&nbsp;Elisa M Valenzuela-Soto,&nbsp;Gloria Yepiz-Plascencia","doi":"10.1007/s10863-023-09960-z","DOIUrl":"https://doi.org/10.1007/s10863-023-09960-z","url":null,"abstract":"<p><p>Animals suffer hypoxia when their oxygen consumption is larger than the oxygen available. Hypoxia affects the white shrimp Penaeus (Litopenaeus) vannamei, both in their natural habitat and in cultivation farms. Shrimp regulates some enzymes that participate in energy production pathways as a strategy to survive during hypoxia. Glucose-6-phosphatase (G6Pase) is key to maintain blood glucose homeostasis through gluconeogenesis and glycogenolysis. We previously reported a shrimp G6Pase gene (G6Pase1) and in this work, we report a second isoform that we named G6Pase2. The expression of the two isoforms was evaluated in oxygen limited conditions and during silencing of the transcription factor HIF-1. High G6Pase activity was detected in hepatopancreas followed by muscle and gills under good oxygen and feeding conditions. Gene expression of both isoforms was analyzed in normoxia, hypoxia and reoxygenation in hepatopancreas and gills, and in HIF-1-silenced shrimp. In fed shrimp with normal dissolved oxygen (DO) (5.0 mg L^- 1 DO) the expression of G6Pase1 was detected in gills, but not in hepatopancreas or muscle, while G6Pase2 expression was undetectable in all three tissues. In hepatopancreas, G6Pase1 is induced at 3 and 48 h of hypoxia, while G6Pase2 is down-regulated in the same time points but in reoxygenation, both due to the knock-down of HIF-1. In gills, only G6Pase1 was detected, and was induced by the silencing of HIF-1 only after 3 h of reoxygenation. Therefore, the expression of the two isoforms appears to be regulated by HIF-1 at transcriptional level in response to oxygen deprivation and subsequent recovery of oxygen levels.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 2","pages":"137-150"},"PeriodicalIF":3.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9921257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant effects of silver nanoparticles obtained by green synthesis from the aqueous extract of Eryngium carlinae on the brain mitochondria of streptozotocin-induced diabetic rats.","authors":"Jenaro Lemus-de la Cruz,&nbsp;Mitchell Trejo-Hurtado,&nbsp;Cinthia Landa-Moreno,&nbsp;Donovan Peña-Montes,&nbsp;José Luis Landeros-Páramo,&nbsp;Christian Cortés-Rojo,&nbsp;Rocío Montoya-Pérez,&nbsp;Gerardo Rosas,&nbsp;Alfredo Saavedra-Molina","doi":"10.1007/s10863-023-09963-w","DOIUrl":"https://doi.org/10.1007/s10863-023-09963-w","url":null,"abstract":"<p><p>Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia that affects practically all tissues and organs, being the brain one of most susceptible, due to overproduction of reactive oxygen species induced by diabetes. Eryngium carlinae is a plant used in traditional Mexican medicine to treat diabetes, which has already been experimentally shown have hypoglycemic, antioxidant and hypolipidemic properties. The green synthesis of nanoparticles is a technique that combines plant extracts with metallic nanoparticles, so that the nanoparticles reduce the absorption and distribution time of drugs or compounds, increasing their effectiveness. In this work, the antioxidant effects and mitochondrial function in the brain were evaluated, as well as the hypoglycemic and hypolipidemic effect in serum of both the aqueous extract of the aerial part of E. carlinae, as well as its combination with silver nanoparticles of green synthesis. Administration with both, extract and the combination significantly decreased the production of reactive oxygen species, lipid peroxidation, and restored the activity of superoxide dismutase 2, glutathione peroxidase, and electron transport chain complexes in brain, while that the extract-nanoparticle combination decreased blood glucose and triglyceride levels. The results obtained suggest that both treatments have oxidative activity and restore mitochondrial function in the brain of diabetic rats.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 2","pages":"123-135"},"PeriodicalIF":3.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9550273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-ascorbic acid could ameliorate the damage of myocardial microvascular endothelial cell caused by hypoxia-reoxygenation via targeting HMGB1.","authors":"Zhanshuai Zhang,&nbsp;Shaoqiang Qin,&nbsp;Yaling Wang,&nbsp;Huiqing Liang,&nbsp;Rui Wang,&nbsp;Fangjiang Li","doi":"10.1007/s10863-023-09962-x","DOIUrl":"https://doi.org/10.1007/s10863-023-09962-x","url":null,"abstract":"<p><p>In this study, we intend to explore the potential function of l-ascorbic acid in hypoxia-reoxygenation (H/R)-induced damage of CMECs and its related molecular mechanism. With different concentrations of l-ascorbic acid treatment, the proliferation, migration, inflammation and autophagy of cardiac microvascular endothelial cells (CMECs) were determined by several biological experiments. Si-HMGB1 transfection was used to reduce HMGB1 expression and to detect the function of HMGB1 in H/R-induced damage of CMECs. Under H/R condition, the proliferation and migration abilities of CMECs were reduced, and the inflammation and autophagy of CMECs were increased. Whereas, after l-ascorbic acid treatment, the reduction in the proliferation and migration of CMECs, as well as the increase in the inflammation and autophagy of CMECs induced by H/R were reversely altered. HMGB1 was confirmed as a specific target of l-ascorbic acid, and si-HMGB1 treatment strengthened the beneficial effect of l-ascorbic acid on H/R-induced damage of CMECs, followed by further reduction in the proliferation and migration abilities of CMECs, as well as the increase in the inflammation and autophagy of CMECs. Few studies have reported the function of l-ascorbic acid in myocardial ischemia on CMECs, but our experimental data showed that l-ascorbic acid treatment could ameliorate the H/R-induced damage of CMECs by regulating HMGB1 expression.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 2","pages":"115-122"},"PeriodicalIF":3.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9603311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diazoxide improves muscle function in association with improved dyslipidemia and decreased muscle oxidative stress in streptozotocin-induced diabetic rats.","authors":"Manuel Alejandro Vargas-Vargas,&nbsp;Alfredo Saavedra-Molina,&nbsp;Mariana Gómez-Barroso,&nbsp;Donovan Peña-Montes,&nbsp;Christian Cortés-Rojo,&nbsp;Alain R Rodríguez-Orozco,&nbsp;Montoya-Pérez Rocío","doi":"10.1007/s10863-023-09958-7","DOIUrl":"https://doi.org/10.1007/s10863-023-09958-7","url":null,"abstract":"<p><strong>Aim/introduction: </strong>Diabetes Mellitus is a chronic degenerative disease, and its main biochemical characteristic is hyperglycemia due to impaired insulin secretion, resistance to peripheral actions of insulin, or both. Hyperglycemia causes dyslipidemia and stimulates oxidative damage, leading to the main symptoms, such as fatigue and culminates in diabetic complications. Previous studies have shown that ATP-sensitive potassium channels counteract muscle fatigue and metabolic stress in healthy mouse models. To determine the effect of diazoxide on muscle strength development during diabetes, we tested the effect of diazoxide in streptozotocin-diabetic rats in muscle function, lipid profile and oxidative stress biomarkers.</p><p><strong>Materials and methods: </strong>Wistar rats were divided into 4 groups of six animals each: (1) Control group, (2) diabetes group, (3) Control group + diazoxide, and (4) Diabetic + diazoxide (DB + DZX). 4 weeks after rats were sacrificed, soleus and extensor digitorum longus muscles (EDL) were extracted to prepare homogenates and serum was obtained for biochemical measurements. Oxidative damage was evaluated by the thiobarbituric acid method and the fluorescent for reactive oxygen species (ROS) probe 2,4-H₂DCFDA, respectively.</p><p><strong>Results: </strong>Diabetic rats with diazoxide administration showed an increase in the development of muscle strength in both muscles; in turn, the onset of fatigue was longer compared to the group of diabetic rats without treatment. Regarding the lipid profile, diazoxide decreased total cholesterol levels in the group of diabetic rats treated with diazoxide (x̅46.2 mg/dL) compared to the untreated diabetic group (x̅=104.4 mg/dL); secondly, diazoxide decreased triglyceride concentrations (x̅=105.3 mg/dL) compared to the untreated diabetic rats (x̅=412.2 mg/dL) as well as the levels of very low-density lipoproteins (x̅=20.4 mg/dL vs. x̅=82.44 mg/dL). Regarding the various markers of oxidative stress, the diabetic group treated with diazoxide was able to reduce the concentrations of TBARS and total reactive oxygen species as well as preserve the concentrations of reduced glutathione.</p><p><strong>Conclusion: </strong>Diazoxide administration in diabetic rats increases muscle strength development in EDL and soleus muscle, decreases fatigue, reduces cholesterol and triglyceride concentrations and improves oxidative stress parameters such as TBARS, ROS, and glutathione status.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 1","pages":"71-78"},"PeriodicalIF":3.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9250324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-coupled receptor 39 alleviates mitochondrial dysfunction and hepatocyte lipid accumulation via SIRT1/Nrf2 signaling.","authors":"Qiang Chen,&nbsp;Yifeng Lou","doi":"10.1007/s10863-022-09953-4","DOIUrl":"https://doi.org/10.1007/s10863-022-09953-4","url":null,"abstract":"<p><strong>Objective: </strong>Data in the GEO database (GSE63067) showed that G protein-coupled receptor 39 (GPR39) was down-regulated in tissues from patients with non-alcoholic fatty liver disease (NAFLD). It was intended to explore the mechanism of GPR39 in NAFLD.</p><p><strong>Methods: </strong>HepG2 cells were treated with a mixture of oleic acid and palmitic acid (OA/PA) to mimic NAFLD cell models. The level of GPR39 and the functions of GPR39 on cellular oxidative stress, lipid accumulation, the SIRT1/Nrf2 signaling and mitochondrial dysfunction were assessed. To verify the mediation of the SIRT1 signaling pathway in GPR39 regulation, cells were subjected to SIRT1 inhibitor EX-527 treatment. Afterwards, the abovementioned aspects of cells were all determined.</p><p><strong>Results: </strong>GPR39 presented a downward trend in response to OA/PA. GPR39 overexpression could suppress oxidative stress, lipid accumulation and activate the SIRT1/Nrf2 signaling. GPR39 overexpression likewise alleviated mitochondrial dysfunction, whereas EX-527 treatment disturbed the effects of GPR39 overexpression on these aspects.</p><p><strong>Conclusion: </strong>The present study found that GPR39 reduced oxidative stress and maintained mitochondrial homeostasis in a cellular model of NAFLD, a process mediated by SIRT1/Nrf2 signaling.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 1","pages":"33-42"},"PeriodicalIF":3.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9249333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Glycolytic inhibitors 2-deoxyglucose and 3-bromopyruvate synergize with photodynamic therapy respectively to inhibit cell migration.","authors":"Xiaolan Feng,&nbsp;Pan Wang,&nbsp;Quanhong Liu,&nbsp;Ting Zhang,&nbsp;Bingjie Mai,&nbsp;Xiaobing Wang","doi":"10.1007/s10863-022-09955-2","DOIUrl":"https://doi.org/10.1007/s10863-022-09955-2","url":null,"abstract":"","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 1","pages":"91-92"},"PeriodicalIF":3.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10782436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caffeine improves mitochondrial function in PINK1^B9-null mutant Drosophila melanogaster.","authors":"Débora F Gonçalves,&nbsp;Leahn R Senger,&nbsp;João V P Foletto,&nbsp;Paula Michelotti,&nbsp;Félix A A Soares,&nbsp;Cristiane L Dalla Corte","doi":"10.1007/s10863-022-09952-5","DOIUrl":"https://doi.org/10.1007/s10863-022-09952-5","url":null,"abstract":"<p><p>Mitochondrial dysfunction plays a central role in Parkinson's disease (PD) and can be triggered by xenobiotics and mutations in mitochondrial quality control genes, such as the PINK1 gene. Caffeine has been proposed as a secondary treatment to relieve PD symptoms mainly by its antagonistic effects on adenosine receptors (ARs). Nonetheless, the potential protective effects of caffeine on mitochondrial dysfunction could be a strategy in PD treatment but need further investigation. In this study, we used high-resolution respirometry (HRR) to test caffeine's effects on mitochondrial dysfunction in PINK1^B9-null mutants of Drosophila melanogaster. PINK1 loss-of-function induced mitochondrial dysfunction in PINK1^B9-null flies observed by a decrease in O₂ flux related to oxidative phosphorylation (OXPHOS) and electron transfer system (ETS), respiratory control ratio (RCR) and ATP synthesis compared to control flies. Caffeine treatment improved OXPHOS and ETS in PINK^B9-null mutant flies, increasing the mitochondrial O₂ flux compared to untreated PINK^B9-null mutant flies. Moreover, caffeine treatment increased O₂ flux coupled to ATP synthesis and mitochondrial respiratory control ratio (RCR) in PINK 1^B9-null mutant flies. The effects of caffeine on respiratory parameters were abolished by rotenone co-treatment, suggesting that caffeine exerts its beneficial effects mainly by stimulating the mitochondrial complex I (CI). In conclusion, we demonstrate that caffeine may improve mitochondrial function by increasing mitochondrial OXPHOS and ETS respiration in the PD model using PINK1 loss-of-function mutant flies.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 1","pages":"1-13"},"PeriodicalIF":3.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9242718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The status and trends of mitochondrial dynamics research: A global bibliometric and visualized analysis.","authors":"Zijian Guo,&nbsp;Zehua Wang,&nbsp;Zhenzhong Gao,&nbsp;Tengda Feng,&nbsp;Yingjie Gao,&nbsp;Zhiwen Yin,&nbsp;Zui Tian,&nbsp;Yang Liu,&nbsp;Xingjia Mao,&nbsp;Chuan Xiang","doi":"10.1007/s10863-023-09959-6","DOIUrl":"https://doi.org/10.1007/s10863-023-09959-6","url":null,"abstract":"<p><strong>Background: </strong>Mitochondria are remarkably dynamic organelles encapsulated by bilayer membranes. The dynamic properties of mitochondria are critical for energy production.</p><p><strong>Aims: </strong>The aim of our study is to investigate the global status and trends of mitochondrial dynamics research and predict popular topics and directions in the field.</p><p><strong>Methods: </strong>Publications related to the studies of mitochondrial dynamics from 2002 to 2021 were retrieved from Web of Science database. A total of 4,576 publications were included. Bibliometric analysis was conducted by visualization of similarities viewer and GraphPadPrism 5 software.</p><p><strong>Results: </strong>There is an increasing trend of mitochondrial dynamics research during the last 20 years. The cumulative number of publications about mitochondrial dynamics research followed the logistic growth model [Formula: see text]. The USA made the highest contributions to the global research. The journal Biochimica et Biophysica Acta (BBA)-Molecular Cell Research had the largest publication numbers. Case Western Reserve University is the most contributive institution. The main research orientation and funding agency were cell biology and HHS. All keywords related studies could be divided into three clusters: \"Related disease research\", \"Mechanism research\" and \"Cell metabolism research\".</p><p><strong>Conclusions: </strong>Attention should be drawn to the latest popular research and more efforts will be put into mechanistic research, which may inspire new clinical treatments for the associated diseases.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"55 1","pages":"43-57"},"PeriodicalIF":3.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9942064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9305209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}