Study: WSTF Protein Can Stop Chronic Inflammation and Treat Obesity

Restoring a specific protein to cells enabled researchers to stop chronic inflammation / ALJAZIRA.net


Chronic inflammation underlies many conditions—from obesity and fatty liver to arthritis and ageing‑associated diseases. A recent study published in Nature shows that restoring the protein WSTF can selectively halt chronic inflammation without impairing the body’s ability to respond to acute threats like infections or injuries.

 What is WSTF?

WSTF (Williams Syndrome Transcription Factor), part of the ISWI chromatin‑remodeling complex, normally resides in the cell nucleus and represses inflammatory genes. During chronic inflammation, a process called “nuclear autophagy” causes WSTF to bind ATG8 proteins and be exported to the cytoplasm, where it is degraded in lysosomes. Loss of nuclear WSTF leads to chromatin opening and persistent inflammatory gene expression .

 Suppressing Chronic But Not Acute Inflammation

The Nature paper demonstrates that:

  • Blocking WSTF–ATG8 binding with cell‑penetrating peptides restores nuclear WSTF levels.
  • This intervention suppresses chronic inflammation in senescent cells, mouse models of metabolic‑dysfunction‑associated steatohepatitis (MASH), and osteoarthritis, without affecting acute inflammatory responses .

 Promising Therapeutic Results

In mouse models, WSTF‑restoring drugs reduced inflammation in livers with fatty liver disease and arthritic joints. In human tissue samples:

  • WSTF was absent in livers from MASH patients but present in healthy controls .
  • Inflamed knee cells from osteoarthritis patients responded to treatment with reduced inflammatory signaling .

 Linking Obesity and Chronic Inflammation

Recent reviews highlight that obesity is characterized by low‑grade chronic inflammation driven by increased pro‑inflammatory cytokines (e.g., TNF‑α, IL‑6, IL‑1β) from hypertrophic adipose tissue, macrophage infiltration, ER stress, and NF‑κB/NLRP3 inflammasome activation .

Targeting WSTF offers a novel approach to break this cycle of inflammation that contributes to insulin resistance, metabolic disease, and obesity.

 Future Research Directions

  • Validate WSTF‑restoring drugs in larger animal studies and preclinical trials.
  • Assess long‑term safety and efficacy in humans.
  • Explore whether similar nuclear‑autophagy mechanisms regulate inflammation in obesity.

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