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HSF1, Aging, and Neurodegeneration.

Alice Y Liu1,2, Conceição A Minetti3, David P Remeta3

  • 1Department of Cell Biology and Neuroscience, Rutgers The State University of New Jersey, Piscataway, NJ, USA. liu@dls.rutgers.edu.

Advances in Experimental Medicine and Biology
|August 22, 2022
PubMed
Summary

Heat shock factor 1 (HSF1) regulates protein quality control, but its function declines with age, contributing to neurodegenerative diseases (ND). Age-related changes in disordered proteins may explain HSF1 dysfunction and aggregate formation in ND.

Keywords:
AgingHSF1, Heat shock factor 1HSP, heat shock protein familyHsp, Specific heat shock proteinIntrinsically disordered proteomeNeurodegenerationProtein homeostasis

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Area of Science:

  • Cellular Biology
  • Neuroscience
  • Biochemistry

Background:

  • Heat shock factor 1 (HSF1) is a key regulator of protein quality control (QC) and proteostasis, crucial for cellular defense against stress.
  • Age-related decline in HSF1 function is implicated in increased vulnerability to neurodegenerative diseases (ND).

Approach:

  • This work reviews the structural, functional, and energetic aspects of HSF1 in healthy cells.
  • It examines the age-dependent deterioration of HSF1 function and neuron-specific susceptibility to ND.
  • The role of intrinsically disordered regions in HSF1 and disease-associated proteins is analyzed.

Key Points:

  • HSF1 orchestrates the induction of heat shock proteins, essential for maintaining proteome integrity.
  • Intrinsically disordered regions are a key feature of HSF1 and many proteins linked to ND.
  • These disordered proteins are sensitive to age-related cellular environment changes.

Conclusions:

  • A hypothesis is proposed: age-dependent alterations in the intrinsically disordered proteome are central to understanding HSF1 dysfunction and protein aggregate formation in ND.
  • This perspective links fundamental aging processes to the molecular pathology of neurodegeneration.