View More View Less
  • 1 Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, PR China
Restricted access

Purchase article

USD  $25.00

1 year subscription (Individual Only)

USD  $752.00

Abstract

Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.

  • 1.

    Pearson JD. Normal endothelial cell function. Lupus 2000; 9: 1838.

  • 2.

    Rodríguez-Iturbe B, Johnson RJ. Heat shock proteins and cardiovascular disease. Physiol Int 2018; 105: 1937.

  • 3.

    Qin W, Xie W, Xia N, He Q, Sun T. Silencing of transient receptor potential channel 4 alleviates oxLDL-induced angiogenesis in human coronary artery endothelial cells by inhibition of VEGF and NF-kappaB. Med Sci Monit 2016; 22: 9306.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4.

    Muller DN, Heissmeyer V, Dechend R, Hampich F, Park JK, Fiebeler A, et al.. Aspirin inhibits NF-kappaB and protects from angiotensin II-induced organ damage. FASEB J 2001; 15: 18224.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Fei Y, Sun L, Yuan C, Jiang M, Lou Q, Xu Y. CFTR ameliorates high glucose-induced oxidative stress and inflammation by mediating the NF-kappaB and MAPK signaling pathways in endothelial cells. Int J Mol Med 2018; 41: 35018.

    • Search Google Scholar
    • Export Citation
  • 6.

    Capodanno D, Angiolillo DJ. Aspirin for primary cardiovascular risk prevention and beyond in diabetes mellitus. Circulation 2016; 134: 157994.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Chang PY, Chen YJ, Chang FH, Lu J, Huang WH, Yang TC, et al.. Aspirin protects human coronary artery endothelial cells against atherogenic electronegative LDL via an epigenetic mechanism: a novel cytoprotective role of aspirin in acute myocardial infarction. Cardiovasc Res 2013; 99: 13745.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Furuno T, Yamasaki F, Yokoyama T, Sato K, Sato T, Doi Y, et al.. Effects of various doses of aspirin on platelet activity and endothelial function. Heart Vessels 2011; 26: 26773.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Ittaman SV, VanWormer JJ, Rezkalla SH. The role of aspirin in the prevention of cardiovascular disease. Clin Med Res 2014; 12: 14754.

  • 10.

    Ou HC, Lee WJ, Wu CM, Chen JF, Sheu WH. Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling. J Vasc Surg 2012; 55: 110415.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Dragomir E, Manduteanu I, Voinea M, Costache G, Manea A, Simionescu M. Aspirin rectifies calcium homeostasis, decreases reactive oxygen species, and increases NO production in high glucose-exposed human endothelial cells. J Diabetes Complications 2004; 18: 28999.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Mehta JL, Chen J, Yu F, Li DY. Aspirin inhibits ox-LDL-mediated LOX-1 expression and metalloproteinase-1 in human coronary endothelial cells. Cardiovasc Res 2004; 64: 2439.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Maejima Y, Isobe M, Sadoshima J. Regulation of autophagy by Beclin 1 in the heart. J Mol Cell Cardiol 2016; 95: 1925.

  • 14.

    McCormick JJ, VanDusseldorp TA, Ulrich CG, Lanphere RL, Dokladny K, Mosely PL, et al.. The effect of aging on the autophagic and heat shock response in human peripheral blood mononuclear cells. Physiol Int 2018; 105: 24756.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Sun X, Du F, Liu S. Modulation of autophagy in exJSRV-env-transfected cells through the Akt/mTOR and MAPK signaling pathway. Biochem Biophys Res Commun 2017; 485: 6728.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Kang R, Zeh HJ, Lotze MT, Tang D. The Beclin 1 network regulates autophagy and apoptosis. Cell Death Differ 2011; 18: 57180.

  • 17.

    Zhao Q, Wang Z, Wang Z, Wu L, Zhang W. Aspirin may inhibit angiogenesis and induce autophagy by inhibiting mTOR signaling pathway in murine hepatocarcinoma and sarcoma models. Oncol Lett 2016; 12: 280410.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Huang Z, Fang W, Liu W, Wang L, Liu B, Liu S, et al.. Aspirin induces Beclin-1-dependent autophagy of human hepatocellular carcinoma cell. Eur J Pharmacol 2018; 823: 5864.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    He D, Zhao M, Wu C, Zhang W, Niu C, Yu B, et al.. Apolipoprotein A-1 mimetic peptide 4F promotes endothelial repairing and compromises reendothelialization impaired by oxidized HDL through SR-B1. Redox Biol 2018; 15: 22842.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Yang L, Cong HL, Wang SF, Liu T. AMP-activated protein kinase mediates the effects of lipoprotein-associated phospholipase A2 on endothelial dysfunction in atherosclerosis. Exp Ther Med 2017; 13: 16229.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Zhang S, Chen L, Zhou Z, Fan W, Liu S. Effects of Puerarin on clinical parameters, vascular endothelial function, and inflammatory factors in patients with coronary artery disease. Med Sci Monit 2019; 25: 4028.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Monobe H, Yamanari H, Nakamura K, Ohe T. Effects of low-dose aspirin on endothelial function in hypertensive patients. Clin Cardiol 2001; 24: 7059.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Kardakaris R, Gareus R, Xanthoulea S, Pasparakis M. Endothelial and macrophage-specific deficiency of P38alpha MAPK does not affect the pathogenesis of atherosclerosis in ApoE-/- mice. PLoS One 2011; 6:e21055.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Chen J, Gong F, Chen MF, Li C, Hong P, Sun S, et al.. In vitro vascular-protective effects of a tilapia by-product oligopeptide on angiotensin II-induced hypertensive endothelial injury in HUVEC by Nrf2/NF-kappaB pathways. Mar Drugs 2019; 17: 431.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Chu P, Han G, Ahsan A, Sun Z, Liu S, Zhang Z, et al.. Phosphocreatine protects endothelial cells from Methylglyoxal induced oxidative stress and apoptosis via the regulation of PI3K/Akt/eNOS and NF-kappaB pathway. Vascul Pharmacol 2017; 91: 2635.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Jayakumar T, Chang CC, Lin SL, Huang YK, Hu CM, Elizebeth AR, et al.. Brazilin ameliorates high glucose-induced vascular inflammation via inhibiting ROS and CAMs production in human umbilical vein endothelial cells. Biomed Res Int 2014; 2014: 403703.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Din FV, Valanciute A, Houde VP, Zibrova D, Green KA, Sakamoto K, et al.. Aspirin inhibits mTOR signaling, activates AMP-activated protein kinase, and induces autophagy in colorectal cancer cells. Gastroenterology 2012; 142: 1504–15.e3.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Hernandez C, Barrachina MD, Vallecillo-Hernandez J, Alvarez A, Ortiz-Masia D, Cosin-Roger J, et al.. Aspirin-induced gastrointestinal damage is associated with an inhibition of epithelial cell autophagy. J Gastroenterol 2016; 51: 691701.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Liu PP, Liu HH, Sun SH, Shi XX, Yang WC, Su GH, et al.. Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy. Acta Pharmacol Sin 2017; 38: 48897.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Levine B, Kroemer G. Autophagy in the pathogenesis of disease. Cell 2008; 132: 2742.

  • 31.

    Xie Y, You SJ, Zhang YL, Han Q, Cao YJ, Xu XS, et al.. Protective role of autophagy in AGE-induced early injury of human vascular endothelial cells. Mol Med Rep 2011; 4: 45964.

    • Search Google Scholar
    • Export Citation
  • 32.

    Wang K, Yang C, Shi J, Gao T. Ox-LDL-induced lncRNA MALAT1 promotes autophagy in human umbilical vein endothelial cells by sponging miR-216a-5p and regulating Beclin-1 expression. Eur J Pharmacol 2019; 858: 172338.

    • Crossref
    • Search Google Scholar
    • Export Citation

 

 

The author instruction is available in PDF.

Please, download the file from HERE

 

 

Editor-in-Chief

László ROSIVALL (Semmelweis University, Budapest, Hungary)

Managing Editor

Anna BERHIDI (Semmelweis University, Budapest, Hungary)

Co-Editors

  • Gábor SZÉNÁSI (Semmelweis University, Budapest, Hungary)
  • Ákos KOLLER (Semmelweis University, Budapest, Hungary)
  • Zsolt RADÁK (University of Physical Education, Budapest, Hungary)
  • László LÉNÁRD (University of Pécs, Hungary)
  • Zoltán UNGVÁRI (Semmelweis University, Budapest, Hungary)

Assistant Editors

  • Gabriella DÖRNYEI (Semmelweis University, Budapest, Hungary)
  • Zsuzsanna MIKLÓS (Semmelweis University, Budapest, Hungary)
  • György NÁDASY (Semmelweis University, Budapest, Hungary)

Hungarian Editorial Board

  • György BENEDEK (University of Szeged, Hungary)
  • Zoltán BENYÓ (Semmelweis University, Budapest, Hungary)
  • Mihály BOROS (University of Szeged, Hungary)
  • László CSERNOCH (University of Debrecen, Hungary)
  • Magdolna DANK (Semmelweis University, Budapest, Hungary)
  • László DÉTÁRI (Eötvös Loránd University, Budapest, Hungary)
  • Zoltán GIRICZ (Semmelweis University, Budapest, Hungary and Pharmahungary Group, Szeged, Hungary)
  • Zoltán HANTOS (Semmelweis University, Budapest and University of Szeged, Hungary)
  • László HUNYADI (Semmelweis University, Budapest, Hungary)
  • Gábor JANCSÓ (University of Pécs, Hungary)
  • Zoltán KARÁDI (University of Pecs, Hungary)
  • Miklós PALKOVITS (Semmelweis University, Budapest, Hungary)
  • Gyula PAPP (University of Szeged, Hungary)
  • Gábor PAVLIK (University of Physical Education, Budapest, Hungary)
  • András SPÄT (Semmelweis University, Budapest, Hungary)
  • Gyula SZABÓ (University of Szeged, Hungary)
  • Zoltán SZELÉNYI (University of Pécs, Hungary)
  • Lajos SZOLLÁR (Semmelweis University, Budapest, Hungary)
  • Gyula TELEGDY (MTA-SZTE, Neuroscience Research Group and University of Szeged, Hungary)
  • József TOLDI (MTA-SZTE Neuroscience Research Group and University of Szeged, Hungary)
  • Árpád TÓSAKI (University of Debrecen, Hungary)

International Editorial Board

  • Dragan DJURIC (University of Belgrade, Serbia)
  • Christopher H.  FRY (University of Bristol, UK)
  • Stephen E. GREENWALD (Blizard Institute, Barts and Queen Mary University of London, UK)
  • Osmo Otto Päiviö HÄNNINEN (Finnish Institute for Health and Welfare, Kuopio, Finland)
  • Helmut G. HINGHOFER-SZALKAY (Medical University of Graz, Austria)
  • Tibor HORTOBÁGYI (University of Groningen, Netherlands)
  • George KUNOS (National Institutes of Health, Bethesda, USA)
  • Massoud MAHMOUDIAN (Iran University of Medical Sciences, Tehran, Iran)
  • Tadaaki MANO (Gifu University of Medical Science, Japan)
  • Luis Gabriel NAVAR (Tulane University School of Medicine, New Orleans, USA)
  • Hitoo NISHINO (Nagoya City University, Japan)
  • Ole H. PETERSEN (Cardiff University, UK)
  • Ulrich POHL (German Centre for Cardiovascular Research and Ludwig-Maximilians-University, Planegg, Germany)
  • Andrej A. ROMANOVSKY (University of Arizona, USA)
  • Anwar Ali SIDDIQUI (Aga Khan University, Karachi, Pakistan)
  • Csaba SZABÓ (University of Fribourg, Switzerland)
  • Eric VICAUT (Université de Paris, UMRS 942 INSERM, France)
  • Nico WESTERHOF (Vrije Universiteit Amsterdam, The Netherlands)

 

Editorial Office:
Akadémiai Kiadó Zrt.
Prielle Kornélia u. 21–35, H-1117 Budapest, Hungary

Editorial Correspondence:
Physiology International
Semmelweis University, Faculty of Medicine Institute of Pathophysiology
Nagyvárad tér 4, H-1089 Budapest, Hungary
Phone/Fax: +36-1-2100-100
E-mail: pi@semmelweis-univ.hu

Indexing and Abstracting Services:

  • Biological Abstracts
  • BIOSIS Previews
  • CAB Abstracts
  • EMBASE/Excerpta Medica
  • Global Health
  • Index Copernicus
  • Index Medicus
  • Medline
  • Referativnyi Zhurnal
  • SCOPUS
  • Social Science Citation Index

 

 

2020  
Total Cites 245
WoS
Journal
Impact Factor
2,090
Rank by Physiology 62/81 (Q4)
Impact Factor  
Impact Factor 1,866
without
Journal Self Cites
5 Year 1,703
Impact Factor
Journal  0,51
Citation Indicator  
Rank by Journal  Physiology 67/84 (Q4)
Citation Indicator   
Citable 42
Items
Total 42
Articles
Total 0
Reviews
Scimago 29
H-index
Scimago 0,417
Journal Rank
Scimago Physiology (medical) Q3
Quartile Score  
Scopus 270/1140=1,9
Scite Score  
Scopus Physiology (medical) 71/98 (Q3)
Scite Score Rank  
Scopus 0,528
SNIP  
Days from  172
submission  
to acceptance  
Days from  106
acceptance  
to publication  

2019  
Total Cites
WoS
137
Impact Factor 1,410
Impact Factor
without
Journal Self Cites
1,361
5 Year
Impact Factor
1,221
Immediacy
Index
0,294
Citable
Items
34
Total
Articles
33
Total
Reviews
1
Cited
Half-Life
2,1
Citing
Half-Life
9,3
Eigenfactor
Score
0,00028
Article Influence
Score
0,215
% Articles
in
Citable Items
97,06
Normalized
Eigenfactor
0,03445
Average
IF
Percentile
12,963
Scimago
H-index
27
Scimago
Journal Rank
0,267
Scopus
Scite Score
235/157=1,5
Scopus
Scite Score Rank
Physiology (medical) 73/99 (Q3)
Scopus
SNIP
0,38

 

Physiology International
Publication Model Hybrid
Submission Fee none
Article Processing Charge 1100 EUR/article
Printed Color Illustrations 40 EUR (or 10 000 HUF) + VAT / piece
Regional discounts on country of the funding agency World Bank Lower-middle-income economies: 50%
World Bank Low-income economies: 100%
Further Discounts Editorial Board / Advisory Board members: 50%
Corresponding authors, affiliated to an EISZ member institution subscribing to the journal package of Akadémiai Kiadó: 100%
Subscription fee 2021 Online subsscription: 632 EUR / 788 USD 
Print + online subscription: 736 EUR / 920 USD
Subscription fee 2022 Online subsscription: 644 EUR / 806 USD
Print + online subscription: 752 EUR / 942 USD
Subscription Information Online subscribers are entitled access to all back issues published by Akadémiai Kiadó for each title for the duration of the subscription, as well as Online First content for the subscribed content.
Purchase per Title Individual articles are sold on the displayed price.

Physiology International
Language English
Size B5
Year of
Foundation
2006 (1950)
Publication
Programme
2021 Volume 108
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 2498-602X (Print)
ISSN 2677-0164 (Online)

Monthly Content Usage

Abstract Views Full Text Views PDF Downloads
Jun 2021 36 2 2
Jul 2021 48 1 2
Aug 2021 85 3 3
Sep 2021 66 1 2
Oct 2021 60 1 1
Nov 2021 62 0 0
Dec 2021 4 0 0