The impact of progredient vessel and tissue stiffening for the development of metabolic syndrome View Full Text


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Article Info

DATE

2022-09-23

AUTHORS

Clemens Loracher, Bruno Märkl, Alois Loracher

ABSTRACT

Established risk factors for the metabolic syndrome as diabetes and arterial hypertension are believed to be the cause of arteriosclerosis and subsequently following diseases like coronary heart disease, apoplexy, or chronic renal failure. Based on broad evidence from the already available experimental literature and clinical experience, an alternative hypothesis is presented that puts an increased vessel and organ stiffness to the beginning of the pathophysiological scenario. The stiffness itself is caused by a persistent activation of mechano-sensitive cation channels like the epithelial/endothelial sodium channel. A further enhancement takes place by proteins like JACD and RhoA coupled phospholipase C coupled G-protein receptors and integrins. A self-enhancing positive feedback loop by activation of YAP/TAZ signaling is a further central pillar of this theory. Further investigations are necessary to verify this hypothesis. If this hypothesis could be confirmed fundamental changes regarding the pharmacologic therapy of the diseases that are currently summarizes as metabolic syndrome would be the consequence. More... »

PAGES

1323-1326

References to SciGraph publications

  • 2014-11-26. Salt controls endothelial and vascular phenotype in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2020-08-21. Insulin: too much of a good thing is bad in BMC MEDICINE
  • 2005-07-16. The myth of the metabolic syndrome in DIABETOLOGIA
  • 2020-04-01. It takes more than two to tango: mechanosignaling of the endothelial surface in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2021-01-04. Pathophysiology-based subphenotyping of individuals at elevated risk for type 2 diabetes in NATURE MEDICINE
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00424-022-02749-w

    DOI

    http://dx.doi.org/10.1007/s00424-022-02749-w

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1151269788

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/36151345


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