Home

Pulmonary Vascular Diseases, especially Pulmonary Arterial Hypertension (PAH), have been the focus of our research effort (Oliveira et al., 2017, 2018, 2019, 2024; Oliveira SD 2022, 2023; Erewele, Castellon, Loya et al., 2022; Marinho, Villarreal et al., 2023; Marinho, Villarreal, Loya, Oliveira, 2024; Silva, Puthanveetil, Oliveira, 2025; Villarreal et al., 2025 – under consideration). PAH is a life-threatening disease highly incident in women, characterized by pulmonary vasoconstriction and vascular remodeling, which elevates the mean PA pressure and leads to right ventricular hypertrophy. Among the signaling pathways contributing to PAH onset, deficiency of pulmonary BMPR2 expression contributes to the hyperactivation of profibrotic TGF-β and vascular remodeling. Although the primary cause of PAH may be multifactorial, studies indicate that it results from chronic pulmonary inflammation. Curiously, infection by the intravascular parasite Schistosoma mansoni recapitulates several aspects of widespread inflammation that lead to PAH, providing a unique model where molecular alterations leading to vascular cell hyperproliferation can be unraveled and hopefully leveraged for the development of clinical solutions for PAH.