Nevertheless, the current study has also potential limitations, since (i) we only assessed MCT-induced animals presenting mild to moderate PAH signs, and did not investigate (ii) how signalling events downstream A2BAR activation could modulate cardiac fibrosis in PAH, nor (iii) did we explore the putative involvement of minority A1AR and/or A3AR in the pro-fibrotic effect of NECA. This evidence concerns the gene ADORA3 and pulmonary arterial hypertension.