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LINK . SPRINGER . COM {}

  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
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s10495-025-02075-3.

Title:
Programmed cardiomyocyte death in myocardial infarction | Apoptosis
Description:
Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI. By gaining a deeper understanding of the mechanisms of cardiomyocyte death, it aims to provide new insights into the prevention and treatment of MI.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Health & Fitness
  • Telecommunications

Content Management System {šŸ“}

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 {šŸ“ˆ}

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {šŸ’ø}

We don't see any clear sign of profit-making.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {šŸ”}

pubmed, article, google, scholar, cas, myocardial, central, cell, infarction, httpsdoiorgs, death, apoptosis, cardiac, wang, autophagy, heart, pathway, biol, ferroptosis, zhang, cardiomyocyte, liu, protein, chen, injury, mol, med, disease, role, sci, pyroptosis, res, kinase, signaling, nature, rev, cardiovascular, cardiomyocytes, factor, ischemiareperfusion, pharmacol, necroptosis, remodeling, exosomes, programmed, mechanisms, promotes, acute, human, necrosis,

Topics {āœ’ļø}

ampk/sirt1/nf-κb signaling pathway tlr4/nf-κb p65 pathway hypoxia/reoxygenation-induced cardiomyocyte injury jnk-drp1-mitochondrial fission pathway month download article/chapter proteins target bcl-xl/mcl-1 pi3k/akt/nrf2/ho-1 signalling mir-138-5p/sirt1 axis ampk/gsk-3β/nrf2 axis mir-15b-5p regulates nlrp3/caspase-1/il-1β pathway tak1/jnk signaling pathway professor meng-nan liu pi3k/akt signaling pathway mesenchymal stem cells cardiac ischaemia-reperfusion injury myocardial ischemia/reperfusion injury myocardial ischemia-reperfusion injury nrf2/ho-1 signaling pathway mir-125b-mediated prevention isoproternol-induced myocardial infraction nlrp3/caspase-1-mediated pyroptosis sarcolemmal ca2+-atpase ability tnf-induced cell death retinoic acid-inducible gene ampk/pgc-1α pathway ros/nlrp3 pyroptosis pathway mir-135b protects cardiomyocytes regulating tsc2-mtor signaling isoprenaline-induced myocardial infarction spatial multi-omic map copper-induced cell death inhibiting nlrp3-induced pyroptosis circadian-regulated cell death ming-tai chen cuproptosis-related gene ube2d3 meng-nan liu ros-ampk-mtor pathway copper-dependent autophagic degradation perk/atf4/chop pathways promoting ripk1-dependent apoptosis inflammasome-activated gasdermin necrostain-1 nf-κb promotes cardiac remodeling programmed cardiomyocyte death hypoxia-induced apoptosis nrf2 signaling pathway hypoxia/reoxygenation hsp70 full article pdf ampk signaling pathway

Questions {ā“}

  • Deans C, Maggert KA (2015) What do you mean, ā€œepigeneticā€?
  • Smith CC, Davidson SM, Lim SY et al (2007) Necrostatin: a potentially novel cardioprotective agent?

Schema {šŸ—ŗļø}

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         headline:Programmed cardiomyocyte death in myocardial infarction
         description:Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI. By gaining a deeper understanding of the mechanisms of cardiomyocyte death, it aims to provide new insights into the prevention and treatment of MI.
         datePublished:2025-01-20T00:00:00Z
         dateModified:2025-01-20T00:00:00Z
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            Cancer Research
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            Biochemistry
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      headline:Programmed cardiomyocyte death in myocardial infarction
      description:Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI. By gaining a deeper understanding of the mechanisms of cardiomyocyte death, it aims to provide new insights into the prevention and treatment of MI.
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         Myocardial infarction
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         Cardiac repair
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         Cell Biology
         Oncology
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         Virology
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                     type:PostalAddress
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      name:Yuan Zou
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            name:Southwest Medical University
            address:
               name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
               type:PostalAddress
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            address:
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               type:PostalAddress
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      email:[email protected]
      name:Ming-Tai Chen
      affiliation:
            name:Guangzhou University of Chinese Medicine
            address:
               name:Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, People’s Republic of China
               type:PostalAddress
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      email:[email protected]
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            name:Southwest Medical University
            address:
               name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
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      name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
      name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
      name:Department of Pediatrics, The Affiliated Hospital, Southwest Medical University, Luzhou, People’s Republic of China
      name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
      name:National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, People’s Republic of China
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      name:Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, People’s Republic of China
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External Links {šŸ”—}(761)

Analytics and Tracking {šŸ“Š}

  • Google Tag Manager

Libraries {šŸ“š}

  • Clipboard.js
  • Prism.js

CDN Services {šŸ“¦}

  • Crossref
  • Pbgrd

5.01s.