Galectin-3 Regulates Smooth Muscle Contraction and Blood Pressure by Modulating Ca V 1.2 Channel Function
Authors' conclusion
These results provide strong evidence that Gal-based CaV1.2 channel modulators are novel therapeutic pathways for normalizing BP.
Study context
- Population
- Transfected HEK 293 cells, isolated smooth muscle cells and arteries from smooth muscle-specific Gal-3 knockout mice and wild-type littermates, spontaneously hypertensive rats, and human patients
- Comparison
- iGal3BP vs amlodipine and losartan
- Outcome
- Molecular mechanisms by which Gal-3 binds to and elevates membrane insertion of CaV1.2 channels, and effect of iGal3BP on BP
Methodological detailsin vitro, ex vivo, in vivo
- In vitro
- Ex vivo
- In vivo
Main finding
As reported in the abstract
Gal-3 modulation of CaV1.2 channel function and BP
- Gal-3 identified as novel binding partner and positive modulator of CaV1.2 via binding to the intracellular II-III loop
- Gal-3 increased total and surface expression, current density and open probability of CaV1.2 channels
- CaV1.2 and Gal-3 upregulated in hypertensive rat aortas and human pulmonary arteries
- Conditional deletion of Gal-3 in smooth muscle markedly lowered CaV1.2 protein and blood pressure (BP) in mice
- iGal3BP significantly reduced BP in spontaneously hypertensive rats by decreasing CaV1.2 protein expression
Further findings
Repeated iGal3BP administration
- Cumulative peptide accumulation in mesenteric arteries and sustained reduction in BP
iGal3BP plus Gal-1 mimetic peptide · within 4 hours; sustained for 35 days
- Sustained BP lowering in hypertensive rats
- 35 days
- SBP returned to normotensive levels within 4 hours
- Negative modulatory Gal-1 mimetic peptide mimicking Gal-1–CaV1.2 interaction
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
Galectin-3 Regulates Smooth Muscle Contraction and Blood Pressure by Modulating Ca V 1.2 Channel Function. Circulation. Published 15 June 2026. doi:10. 1161/ circulationaha. 126. 080022
Summarised from the published abstract; every number is checked against it