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Heat Shock Factor 2 Protects against Proteotoxicity by Maintaining Cell-Cell Adhesion, 2020, Joutsen et al

Discussion in ''Conditions related to ME/CFS' news and research' started by Hoopoe, Jul 8, 2022.

  1. Hoopoe

    Hoopoe Senior Member (Voting Rights)

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    • HSF2 is required to maintain cell-cell adhesion
    • HSF2 deficiency leads to downregulation of cadherin superfamily genes
    • Impaired cell-cell adhesion sensitizes cells to prolonged proteotoxic stress
    • Cadherin-mediated cell-cell adhesion is a survival determinant upon proteotoxicity
    https://www.cell.com/cell-reports/fulltext/S2211-1247(19)31694-8

    This suggests that the increased expression of cadherins in ME/CFS might be a response to a specific type of stressor. Has HSF2 been studied in ME/CFS?
     
  2. Midnattsol

    Midnattsol Moderator Staff Member

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    AliceLily, Hutan, alktipping and 2 others like this.
  3. Hutan

    Hutan Moderator Staff Member

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    I do think that cadherins are worth looking at more.

    Toxins from some dinoflagellates disrupt cadherin function. This may be a mode of action in ciguatera fish poisoning (CFP). Some people affected by CFP go on to develop a chronic illness that is a lot like ME/CFS. (I haven't looked into this in detail, but just wanted to note the potential similarity.)
     
  4. Hoopoe

    Hoopoe Senior Member (Voting Rights)

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    Something like heat shock proteins being dysregulated might explain the poor stress and exertion tolerance of patients (they don't just protect cells against heat shock but against many types of stressors).
     
    Last edited: Jul 9, 2022
    Sean likes this.
  5. Midnattsol

    Midnattsol Moderator Staff Member

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    Yes :) There are some more studies from around the same time period as the one I posted above, though if I remember correctly they are all small and criteriria for diagnosis doesn't contain PEM.
     

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