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  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/s00018-020-03694-6.

Title:
The regulatory roles of p53 in cardiovascular health and disease | Cellular and Molecular Life Sciences
Description:
Cardiovascular disease (CVD) remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for its prevention. The transcription factor p53 functions as a gatekeeper, regulating a myriad of genes to maintain normal cell functions. It has received a great deal of research attention as a tumor suppressor. In the past three decades, evidence has also shown a regulatory role for p53 in the heart. Basal p53 is essential for embryonic cardiac development; it is also necessary to maintain normal heart architecture and physiological function. In pathological cardiovascular circumstances, p53 expression is elevated in both patient samples and animal models. Elevated p53 plays a regulatory role via anti-angiogenesis, pro-programmed cell death, metabolism regulation, and cell cycle arrest regulation. This largely promotes the development of CVDs, particularly cardiac remodeling in the infarcted heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, and diabetic cardiomyopathy. Roles for p53 have also been found in atherosclerosis and chemotherapy-induced cardiotoxicity. However, it has different roles in cardiomyocytes and non-myocytes, even in the same model. In this review, we describe the different effects of p53 in cardiovascular physiological and pathological conditions, in addition to potential CVD therapies targeting p53.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {๐Ÿ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {๐Ÿ“}

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 {๐Ÿ“ˆ}

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

๐ŸŒ  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? {๐Ÿ’ธ}

We're unsure if the website is profiting.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {๐Ÿ”}

pubmed, article, google, scholar, cas, central, cell, wang, heart, apoptosis, cardiac, zhang, liu, biol, death, myocardial, sci, disease, cardiomyopathy, res, nat, mol, regulation, httpsdoiorgs, chen, mitochondrial, circ, circulation, physiol, cai, role, dysfunction, cardiovascular, atherosclerosis, med, protein, cells, zhou, factor, protects, mice, nature, cardiol, endothelial, diabetic, inhibition, senescence, regulates, injury, autophagy,

Topics {โœ’๏ธ}

pten-phosphatidylinositol 3-kinase-akt-dependent manner month download article/chapter von hippel-lindau protein hypoxia-inducible factor-1 alpha mitochondrial apoptosis-inducing factor gene-environment interaction impacts dna-mediated charge transport post-infarct cardiac remodeling partial research-related expenses cytoskeletal protein alpha-actinin mesenchymal-endothelial transition contributes p53-mediated dark skin p53/jnk-mediated apoptosis preventing early-stage apoptosis lkb1-ampk pathway o2-regulated prolyl hydroxylation writingโ€”original draft preparation doxorubicin-induced mitochondrial dysfunction cell cycle arrest pml-dependent p53 activation endothelial growth arrest growth factor receptor hif-1{alpha} prevents deterioration mdm2-p53 relationship evolves p53-dependent dilated cardiomyopathy hypoxia-inducible factor 1 full article pdf pacing-induced heart failure pro-programmed cell death mitochondrial permeability transition dna-bound protein endoplasmic reticulum stress streptozotocin-induced diabetic mice p53 dependent pathway p53-dependent pathway ca2+-dependent manner pediatric research institute cancer therapy-induced cardiotoxicity forkhead box o3a exacerbate cardiac damage dj-1-deficient zebrafish model pifithrin-alpha protects p53-dependent apoptosis early-onset heart failure p53-regulated genes leading promoting myocardial angiogenesis pathological cardiovascular circumstances increased oxidative metabolism hypoxia-inducible factors cardiac gene expression

Schema {๐Ÿ—บ๏ธ}

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         headline:The regulatory roles of p53 in cardiovascular health and disease
         description:Cardiovascular disease (CVD) remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for its prevention. The transcription factor p53 functions as a gatekeeper, regulating a myriad of genes to maintain normal cell functions. It has received a great deal of research attention as a tumor suppressor. In the past three decades, evidence has also shown a regulatory role for p53 in the heart. Basal p53 is essential for embryonic cardiac development; it is also necessary to maintain normal heart architecture and physiological function. In pathological cardiovascular circumstances, p53 expression is elevated in both patient samples and animal models. Elevated p53 plays a regulatory role via anti-angiogenesis, pro-programmed cell death, metabolism regulation, and cell cycle arrest regulation. This largely promotes the development of CVDs, particularly cardiac remodeling in the infarcted heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, and diabetic cardiomyopathy. Roles for p53 have also been found in atherosclerosis and chemotherapy-induced cardiotoxicity. However, it has different roles in cardiomyocytes and non-myocytes, even in the same model. In this review, we describe the different effects of p53 in cardiovascular physiological and pathological conditions, in addition to potential CVD therapies targeting p53.
         datePublished:2020-11-11T00:00:00Z
         dateModified:2020-11-11T00:00:00Z
         pageStart:2001
         pageEnd:2018
         sameAs:https://doi.org/10.1007/s00018-020-03694-6
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            Cardiovascular disease
            Apoptosis
            Angiogenesis
            Metabolism
            Cell cycle arrest
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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               name:Yang Zheng
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      headline:The regulatory roles of p53 in cardiovascular health and disease
      description:Cardiovascular disease (CVD) remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for its prevention. The transcription factor p53 functions as a gatekeeper, regulating a myriad of genes to maintain normal cell functions. It has received a great deal of research attention as a tumor suppressor. In the past three decades, evidence has also shown a regulatory role for p53 in the heart. Basal p53 is essential for embryonic cardiac development; it is also necessary to maintain normal heart architecture and physiological function. In pathological cardiovascular circumstances, p53 expression is elevated in both patient samples and animal models. Elevated p53 plays a regulatory role via anti-angiogenesis, pro-programmed cell death, metabolism regulation, and cell cycle arrest regulation. This largely promotes the development of CVDs, particularly cardiac remodeling in the infarcted heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, and diabetic cardiomyopathy. Roles for p53 have also been found in atherosclerosis and chemotherapy-induced cardiotoxicity. However, it has different roles in cardiomyocytes and non-myocytes, even in the same model. In this review, we describe the different effects of p53 in cardiovascular physiological and pathological conditions, in addition to potential CVD therapies targeting p53.
      datePublished:2020-11-11T00:00:00Z
      dateModified:2020-11-11T00:00:00Z
      pageStart:2001
      pageEnd:2018
      sameAs:https://doi.org/10.1007/s00018-020-03694-6
      keywords:
         p53
         Cardiovascular disease
         Apoptosis
         Angiogenesis
         Metabolism
         Cell cycle arrest
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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                  name:First Hospital of Jilin University, Jilin University
                  address:
                     name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
                     type:PostalAddress
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            name:Wenqian Zhou
            affiliation:
                  name:First Hospital of Jilin University, Jilin University
                  address:
                     name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
                     type:PostalAddress
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                     type:PostalAddress
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            name:Xiang Wang
            affiliation:
                  name:First Hospital of Jilin University, Jilin University
                  address:
                     name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
                     type:PostalAddress
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                  name:Pediatric Research Institute, University of Louisville
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                     name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
                     type:PostalAddress
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            affiliation:
                  name:First Hospital of Jilin University, Jilin University
                  address:
                     name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
                     type:PostalAddress
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                  name:Pediatric Research Institute, University of Louisville
                  address:
                     name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
                     type:PostalAddress
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            name:Yang Zheng
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                  name:First Hospital of Jilin University, Jilin University
                  address:
                     name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
                     type:PostalAddress
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            email:[email protected]
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            name:Lu Cai
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         name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
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      address:
         name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
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               type:PostalAddress
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            name:Pediatric Research Institute, University of Louisville
            address:
               name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
               type:PostalAddress
            type:Organization
      name:He Cai
      affiliation:
            name:First Hospital of Jilin University, Jilin University
            address:
               name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
               type:PostalAddress
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      name:Quanli Cheng
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            name:First Hospital of Jilin University, Jilin University
            address:
               name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
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            name:First Hospital of Jilin University, Jilin University
            address:
               name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
               type:PostalAddress
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            name:First Hospital of Jilin University, Jilin University
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            type:Organization
      name:Shan Huang
      affiliation:
            name:First Hospital of Jilin University, Jilin University
            address:
               name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
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            address:
               name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
               type:PostalAddress
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      email:[email protected]
      name:Lu Cai
      url:http://orcid.org/0000-0003-3048-1135
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            address:
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      name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
      name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
      name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
      name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
      name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
      name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
      name:Department of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, USA
      name:Department of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, China
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      name:Department of Pharmacology and Toxicology, University of Louisville, Louisville, USA
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External Links {๐Ÿ”—}(811)

Analytics and Tracking {๐Ÿ“Š}

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