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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s00395-017-0628-z.

Title:
Exercise-induced circulating extracellular vesicles protect against cardiac ischemia–reperfusion injury | Basic Research in Cardiology
Description:
Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice. However, injection of exercise-induced EVs in a quantity equivalent to the increase seen with exercise (1.85 swim group) significantly enhanced the protective effect. Similarly, treatment with exercise-induced increased EVs provided additional anti-apoptotic effect in H2O2-treated H9C2 cardiomyocytes mediated by the activation of ERK1/2 and HSP27 signaling. Finally, by treating H9C2 cells with insulin-like growth factor-1 to mimic exercise stimulus in vitro, we found an increased release of EVs from cardiomyocytes associated with ALIX and RAB35 activation. Collectively, our results show that exercise-induced increase in circulating EVs enhances the protective effects of endogenous EVs against cardiac I/R injury. Exercise-derived EVs might serve as a potent therapy for myocardial injury in the future.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • Fitness & Wellness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,432 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

pubmed, article, google, scholar, cas, central, cardiac, injury, extracellular, vesicles, exercise, exerciseinduced, xiao, cell, zhang, res, evs, heart, myocardial, physiol, chen, basic, ischemiareperfusion, exosomes, apoptosis, cardiol, access, cardiovascular, dois, research, circulating, che, cells, role, wang, protects, privacy, cookies, function, content, cardioprotection, mice, diseases, regulation, muscle, mol, yellon, kim, biogenesis, biol,

Topics {✒️}

endurance exercise-derived exosomes month download article/chapter exercise-induced adipo-myokines cardiac ischemia–reperfusion injury exercise-induced cardiac growth myocardial ischemia–reperfusion injury cardiac extracellular vesicles hydrogen peroxide-mediated injury prevent cardiomyocyte apoptosis carbrera-fuentes ha small extracellular vesicles article basic research myoblast-myotube cross talk exercise-derived evs human skeletal muscle exercise-induced stress circulating evs enhances full article pdf ischemia–reperfusion injury ischemia/reperfusion injury hausenloy dj extracellular vesicles improve cardiac function acute ischemia/reperfusion h9c2 cells treated exercise-induced evs privacy choices/manage cookies exercise-induced production cardiac cell proliferation ischaemia/reperfusion injury ischaemia-reperfusion injury related subjects links skeletal muscle ravi shah exercise-induced increase treat metabolic diseases treating h9c2 cells state key laboratory cardiac myocyte exosomes enhance cardiac function targeting reperfusion injury cell mol med plasma exosomes protect protects h9c2 cells references aoi mir-17-3p contributes akt-mediated mechanism acute myocardial infarction harvard medical school apoptosis induced

Questions {❓}

  • Aoi W, Sakuma K (2014) Does regulation of skeletal muscle function involve circulating microRNAs?
  • Forterre A, Jalabert A, Berger E, Baudet M, Chikh K, Errazuriz E, De Larichaudy J, Chanon S, Weiss-Gayet M, Hesse AM, Record M, Geloen A, Lefai E, Vidal H, Coute Y, Rome S (2014) Proteomic analysis of C2C12 myoblast and myotube exosome-like vesicles: a new paradigm for myoblast-myotube cross talk?

Schema {🗺️}

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         description:Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice. However, injection of exercise-induced EVs in a quantity equivalent to the increase seen with exercise (1.85 swim group) significantly enhanced the protective effect. Similarly, treatment with exercise-induced increased EVs provided additional anti-apoptotic effect in H2O2-treated H9C2 cardiomyocytes mediated by the activation of ERK1/2 and HSP27 signaling. Finally, by treating H9C2 cells with insulin-like growth factor-1 to mimic exercise stimulus in vitro, we found an increased release of EVs from cardiomyocytes associated with ALIX and RAB35 activation. Collectively, our results show that exercise-induced increase in circulating EVs enhances the protective effects of endogenous EVs against cardiac I/R injury. Exercise-derived EVs might serve as a potent therapy for myocardial injury in the future.
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      headline:Exercise-induced circulating extracellular vesicles protect against cardiac ischemia–reperfusion injury
      description:Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice. However, injection of exercise-induced EVs in a quantity equivalent to the increase seen with exercise (1.85 swim group) significantly enhanced the protective effect. Similarly, treatment with exercise-induced increased EVs provided additional anti-apoptotic effect in H2O2-treated H9C2 cardiomyocytes mediated by the activation of ERK1/2 and HSP27 signaling. Finally, by treating H9C2 cells with insulin-like growth factor-1 to mimic exercise stimulus in vitro, we found an increased release of EVs from cardiomyocytes associated with ALIX and RAB35 activation. Collectively, our results show that exercise-induced increase in circulating EVs enhances the protective effects of endogenous EVs against cardiac I/R injury. Exercise-derived EVs might serve as a potent therapy for myocardial injury in the future.
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            name:Harvard Medical School
            address:
               name:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Ionita Ghiran
      affiliation:
            name:Harvard Medical School
            address:
               name:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Ravi Shah
      affiliation:
            name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School
            address:
               name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Yongqin Li
      affiliation:
            name:Shanghai University
            address:
               name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Yuhui Zhang
      affiliation:
            name:National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College
            address:
               name:Heart Failure Care Unit, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
               type:PostalAddress
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      name:Saumya Das
      affiliation:
            name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School
            address:
               name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Junjie Xiao
      affiliation:
            name:Shanghai University
            address:
               name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
      name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
      name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
      name:Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
      name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, USA
      name:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
      name:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
      name:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
      name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, USA
      name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
      name:Heart Failure Care Unit, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
      name:Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, USA
      name:Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai, China
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