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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Sotatercept Reverses SIN3a Deficiency-Driven PAH by Reprogramming BMPR2/TGF-β-HIF-1α Signaling Pathways.

Katherine Jankowski1, Anurupa Ghosh1, Maria T Ochoa2

  • 1Department of Pharmacological Sciences, Icahn School of Medicine, Mount Sinai, New York, NY 10029, USA.

Biorxiv : the Preprint Server for Biology
|February 12, 2026
PubMed
Summary
This summary is machine-generated.

Switch-independent 3a (SIN3a) loss accelerates pulmonary arterial hypertension (PAH) by disrupting BMPR2 signaling. Sotatercept treatment reverses PAH, restoring SIN3a and BMPR2 expression, highlighting SIN3a as a therapeutic target.

Keywords:
BMPR2 signalingPulmonary arterial hypertensionSotaterceptTGF-β signalingvascular remodeling

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Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Epigenetics

Background:

  • Pulmonary arterial hypertension (PAH) involves pulmonary artery smooth muscle cell (PASMC) proliferation and vascular remodeling.
  • Dysregulated BMPR2 signaling and suppressed BMPR2 expression are hallmarks of PAH.
  • The role of Switch-independent 3a (SIN3a) in PAH pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the role of SIN3a in PAH pathogenesis.
  • To determine if SIN3a regulates BMPR2 expression and signaling in PASMCs.
  • To evaluate the therapeutic potential of targeting SIN3a or related pathways in PAH.

Main Methods:

  • Generated smooth muscle cell-specific SIN3a knockout mice (SIN3a SMC-/-) and induced PAH using the Sugen/hypoxia protocol.
  • Treated a cohort of mice with Sotatercept.
  • Overexpressed SIN3a in human PASMCs and exposed them to TGFβ1 or hypoxia in vitro.
  • Performed transcriptomic profiling, pathway analyses, hemodynamic measurements, and morphometric analyses.

Main Results:

  • SIN3a overexpression in PASMCs restored BMPR2 expression and activated BMP signaling while suppressing pro-inflammatory and fibrotic pathways.
  • SIN3a and Sotatercept converge on gene networks regulating BMPR2 signaling, oxidative stress, and inflammation.
  • SIN3a deficiency exacerbated PAH in vivo, while Sotatercept treatment reversed pathological features and restored SIN3a/BMPR2 expression.

Conclusions:

  • SIN3a is a critical epigenetic regulator of PASMC homeostasis, integrating oxidative stress, inflammation, and fibrotic signaling.
  • Loss of SIN3a accelerates PAH progression; Sotatercept restores SIN3a expression and rebalances signaling pathways.
  • SIN3a is a therapeutic target, and Sotatercept shows promise as a disease-modifying treatment for pulmonary vascular disease.