Cardiac desmosomes are specialized cell junctions responsible for cardiomyocytes mechanical coupling. Mutation in desmosomal genes cause autosomal dominant and recessive familial arrhythmogenic cardiomyopathy. Motivated by evidence that Mendelian diseases share genetic architecture with common complex traits, we assessed whether common variants in any desmosomal gene were associated with cardiac conduction traits in the general population. We analysed data of N=4342 Cooperative Health Research in South Tyrol (CHRIS) study participants. We tested associations between genotype imputed variants covering the five desmosomal genes and and P-wave, PR, QRS, and QT electrocardiographic intervals, using linear mixed models. Functional annotation and interrogation of publicly available genome-wide association study resources implicated potential connection with antisense lncRNAs, DNA methylation sites, and complex traits. Causality was tested via two-sample Mendelian randomization (MR) analysis and validated with functional follow-up in human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs). variant rs2744389 was associated with QRS (=3.5×10), with replication in the Microisolates in South Tyrol (MICROS) study (n=636; =0.010). Observing that rs2744389 was associated with antisense lncRNA but not with expression in multiple GTEx-v8 tissues, we conducted two-sample Mendelian randomization analyses that identified causal effects of on expression (=6.33×10; colocalization posterior probability=0.91) and QRS (=0.015). In hiPSC-CMs, expression downregulation through a specific GapmerR matching sequence led to significant upregulation at both mRNA and protein levels. The evidence that has a regulatory role on opens the venue for further investigations on 's therapeutic potential for conditions caused by reduced desmoplakin production.