Key result
Conductive GelMA/PEDOT:PSS hydrogel boosts cardiomyocyte conduction velocity by ~52% and upregulates gap junctions.
Why the study?
Atrial fibrillation is characterized by electrical remodeling driven by disrupted Cx43-mediated intercellular coupling and aberrant KV1.5 channel regulation. A conductive GelMA/PEDOT:PSS hydrogel was engineered to restore atrial electrical coupling and suppress AF-associated electrophysiological dysfunction.
Does a conductive GelMA/PEDOT:PSS hydrogel restore Cx43-dependent KV1.5 regulation and improve electrical remodeling in an experimental model of atrial fibrillation?
Does a conductive GelMA/PEDOT:PSS hydrogel restore Cx43-dependent KV1.5 regulation and improve electrical remodeling in an experimental model of atrial fibrillation?
Conductive GelMA/PEDOT:PSS hydrogels rescue Cx43-dependent KV1.5 regulation and reverse atrial electrical remodeling in vitro with no in vivo systemic toxicity, offering a potential non-pharmacological biomaterial platform for atrial fibrillation.
Answers are grounded in this paper and cite their sources.
May aid atrial conduction in vitro; hypothesis-generating for conductive hydrogels in AF remodeling, requiring in vivo validation.
Atrial fibrillation (AF) is characterized by electrical remodeling driven by disrupted Connexin‐43 (Cx43)‐mediated intercellular coupling and aberrant KV1.5 channel regulation. Here, we engineered a conductive gelatin methacryloyl (GelMA)/PEDOT:PSS hydrogel to restore atrial electrical coupling and suppress AF‐associated electrophysiological dysfunction. PEDOT:PSS incorporation increased the electrical conductivity of the GelMA hydrogel from 0.05 to 0.83 S cm −1 , corresponding to an approximately 16‐fold enhancement. The GelMA/PEDOT:PSS hydrogels exhibited moduli ranging from approximately 0.20 to 5.2 kPa. The conductive hydrogel exhibited a lower swelling ratio (~28%) and lower enzymatic degradation rates than the GelMA controls. In vitro studies performed on HL‐1 atrial cardiomyocytes showed that GelMA/PEDOT:PSS treatment significantly increased Cx43 (GJA1) and KV1.5 (KCNA5) gene expression by 2.4‐fold and 1.9‐fold, respectively, compared to AF‐like controls ( p < 0.01). Electrophysiological studies showed significant improvement in electrical properties with a ~52% increase in conduction velocity and ~42% reduction in repolarization heterogeneity. Furthermore, the specific knockdown of the Cx43 gene prevented the normalization of KV1.5 and the electrical recovery induced by the hydrogel, suggesting that this process is Cx43‐dependent. In vivo implantation of GelMA/PEDOT:PSS hydrogels showed no systemic toxicity and good biodistribution with no accumulation in organs. Taken together, these data suggest that conductive GelMA/PEDOT:PSS hydrogels rescue the Cx43‐dependent regulation of KV1.5 and therefore improve atrial electrical remodeling. This biomaterial‐based strategy offers a non‐pharmacological therapeutic platform for the treatment of atrial fibrillation.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2026) studied Atrial fibrillation (in vitro HL-1 atrial cardiomyocytes and in vivo preclinical model). Conductive GelMA/PEDOT:PSS hydrogel vs. GelMA controls and AF-like controls was evaluated on Cx43 (GJA1) and KV1.5 (KCNA5) gene expression, conduction velocity, and repolarization heterogeneity (2.4-fold increase in Cx43 and 1.9-fold increase in KV1.5 expression, p=<0.01). Conductive GelMA/PEDOT:PSS hydrogel increased Cx43 by 2.4-fold and KV1.5 by 1.9-fold, increasing conduction velocity by ~52% in HL-1 atrial cardiomyocytes.
Synapse has enriched 10 related papers. Consider them for comparative context: