ArticleMolecular and cellular biochemistry2026
SMAD3 phosphorylation inhibitor, tomentosenol A arrests cell cycle progression and induces apoptotic signalling in cultured fibroblasts: implications for anti-scarring activity.
Article in Molecular and cellular biochemistry, 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
Hypertrophic scars are characterised by excessive fibroblast proliferation, myofibroblast activation, aberrant extracellular matrix deposition and reduced apoptosis. Current anti-scar therapies have variable efficacy and are limited by recurrence, tissue damage and pain, so new strategies are needed. In this study, we examined the efficacy of tomentosenol A, a meroterpenoid compound isolated from Australian stingless bee propolis, to intervene in the development of the cellular hallmarks of scar tissue. The effects of tomentosenol A were compared to two structural analogues (4S)- and (4R)-ficifolidione, using cultured HEK293 cells expressing a SMAD binding element/secreted embryonic alkaline phosphatase reporter and cultured normal adult human dermal fibroblasts. Cell cycle progression was assessed by CDK2 (Tyr15) and Histone H3 (Ser10) phosphorylation, apoptotic signalling by caspase-3/7 activity, and fibroblast wound closure by live-cell scratch-wound assay. The findings revealed that all compounds inhibited TGF-β1-stimulated fibroblast activation, as evidenced by prevention of α-smooth muscle actin assembly in cytoskeletal microfilaments, but only tomentosenol A prevented TGF-β1-stimulated SMAD signalling and fibronectin secretion. Tomentosenol A stimulated G1/S transition and arrested cells at G2/M; (4S)-ficifolidione was without effect on cell cycle progression while (4R)-ficifolidione arrested cells at G1/S. Only tomentosenol A stimulated caspase-3/7 activity, and this effect was attenuated by TGF-β1. Tomentosenol A also concentration-dependently slowed fibroblast wound closure. The findings establish tomentosenol A as a lead compound to test for anti-scarring activity. The structure in the vicinity of the free syncarpic acid conjugated with a pinene moiety appears critical to the anti-scarring potential of tomentosenol A.
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