Age-related remodeling of the JAK/STAT/SOCS signaling pathway and associated myocardial changes: From histological to

Basma Emad Aboulhoda1

  • 1Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Egypt.

Abstract

Insights

Aging hearts show structural changes like hypertrophy, fibrosis, and inflammation. The JAK/STAT/SOCS pathway is altered, with declining JAK/STAT and increasing SOCS3, offering potential therapeutic targets for age-related heart disease.

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Mechanisms of Disease

Background:

  • Age-associated myocardial structural changes impact cardiac function and are targets for intervention.
  • The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) and Suppressor of Cytokine Signaling (SOCS) pathway is implicated in these age-related alterations.

Purpose of the Study:

  • To investigate age-dependent changes in rat myocardium.
  • To establish a morphological basis for age-related myocardial hypertrophy, fibrosis, and inflammation.

Main Methods:

  • Used Sprague Dawley rats across three age groups (6, 30, 36 months).
  • Performed gross, microscopic (H&E, Masson's trichrome), and immunohistochemical analyses (JAK, pSTAT3, α-SMA, β-MHC, CD45).
  • Conducted Western blotting (SOCS), RT-PCR (TNFα, IL1β, α-SKA), biochemical assays (cardiac troponin I, CK-MB), and electron microscopy (capillary density).

Main Results:

  • JAK and pSTAT3 nuclear localization decreased with age; SOCS3 activity increased.
  • Aged myocardium exhibited significant structural changes, including hypertrophy, fibrosis, and inflammation in senile and very senile rats.

Conclusions:

  • Age-related modifications in the JAK/STAT/SOCS pathway are linked to pathological myocardial changes.
  • These findings offer insights into age-associated heart pathologies and potential cardioprotective targets.

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