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Related Experiment Video

Updated: Nov 15, 2025

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Endogenous SO2-dependent Smad3 redox modification controls vascular remodeling.

Yaqian Huang1, Zongmin Li2, Lulu Zhang1

  • 1Department of Pediatrics, Peking University First Hospital, Beijing, 100034, China.

Redox Biology
|March 1, 2021
PubMed
Summary

Sulfur dioxide (SO2) activates hydrogen peroxide (H2O2) to modify proteins, revealing a new signaling pathway. This SO2-mediated cysteine sulfenylation impacts vascular smooth muscle cells and Smad3 activity, influencing hypertension.

Keywords:
CysteineSO(2)Smad3SulfenylationVascular remodeling

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Sulfur dioxide (SO2) is a key signaling molecule in vascular function.
  • The precise molecular mechanisms of SO2 action remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which SO2 regulates its upstream targets.
  • To investigate the role of SO2 in vascular pathophysiology.

Main Methods:

  • Site-centric chemoproteomics was employed to identify SO2-mediated protein modifications.
  • Analysis of cysteine sulfenylation events in vascular smooth muscle cells.
  • Investigated the impact of Smad3 sulfenylation on DNA binding and cellular responses.

Main Results:

  • SO2 facilitates the conversion of H2O2 to peroxymonosulfite, enabling cysteine sulfenylation.
  • >1000 sulfenylation events were identified, with ~42% dynamically regulated by SO2.
  • Sulfenylation of Smad3 at Cys64 inhibited its DNA binding and attenuated SO2's protective effects against angiotensin II-induced vascular remodeling.

Conclusions:

  • SO2 exerts its vascular effects through a redox-dependent mechanism involving cysteine sulfenylation.
  • Smad3 sulfenylation is a critical SO2-mediated event influencing vascular remodeling and hypertension.
  • This study reveals a novel pathway for SO2 signaling in the vasculature.