ArticleFrontiers in pharmacology2026
Resolvin D1 attenuates pulmonary hypertension by suppressing pathological connexin 43-mediated gap junctional communication in pulmonary arterial smooth muscle cells.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pulmonary hypertension (PH) is characterized by progressive pulmonary vascular remodeling driven by activation of pulmonary arterial smooth muscle cells (PASMCs). Resolvin D1 (RvD1), a specialized pro-resolving lipid mediator derived from docosahexaenoic acid (DHA), has vascular protective actions; however, its pharmacological effect on connexin 43 (Cx43)-mediated gap junctional intercellular communication in PH remains unclear. This study investigated whether RvD1 attenuates PH by suppressing pathological formation of gap-junctional Cx43 (GJs-Cx43) in PASMCs. Methods: SU5416/hypoxia-induced PH was established in C57BL/6 mice. Results: RvD1 improved pulmonary hemodynamics and right ventricular adaptation in SU5416/hypoxia-exposed mice. RvD1 also reduced pulmonary arterial wall thickening, elastic lamina remodeling, α-SMA accumulation and PCNA-positive proliferating cells. Mechanistically, SU5416/hypoxia increased total Cx43 and shifted Cx43 toward the GJs-Cx43 formation. RvD1 inhibited GJs-Cx43 formation and attenuated IL-1β, IL-6, ROS and MDA accumulation while partially restoring SOD. In primary PASMCs, hypoxia increased GJs-Cx43 expression, enhanced lucifer yellow dye transfer, and promoted proliferation and migration; these changes were suppressed by RvD1. ZP1609 restored GJs-Cx43-mediated intercellular communication and weakened the inhibitory effects of RvD1 on PASMC inflammatory activation, oxidative stress, proliferation and migration. Conclusion: Pathological GJs-Cx43 formation promotes the spread of remodeling-associated signals across PASMCs networks. RvD1 limits pulmonary vascular remodeling by suppressing Cx43-dependent gap junctional communication, identifying GJs-Cx43 as a pharmacologically relevant mechanism underlying the vascular protection afforded by this DHA-derived lipid mediator.
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