Publications by authors named "Celina De Almeida"
Article Synopsis
- Losing a protein called PPARγ makes a condition called pulmonary arterial hypertension (PAH) worse, but boosting it can help reduce the problem.
- A diabetes medication called Empagliflozin (Empa) was tested and showed it can slow down the growth of bad cells in PAH.
- Empa works by helping PPARγ to control other proteins that are involved in the disease, making it a possible new treatment for PAH.
The loss of semaphorin 3A (Sema3A), which is related to endothelial-to-mesenchymal transition (EndMT) in atrial fibrosis, is implicated in the pathogenesis of atrial fibrillation (AF). To explore the mechanisms by which EndMT affects atrial fibrosis and assess the potential of a Sema3A activator (naringin) to prevent atrial fibrosis by targeting transforming growth factor-beta (TGF-β)-induced EndMT, we used human atria, isolated human atrial endocardial endothelial cells (AEECs), and used transgenic mice expressing TGF-β specifically in cardiac tissues (TGF-β transgenic mice). We evaluated an EndMT marker (Twist), a proliferation marker (proliferating cell nuclear antigen; PCNA), and an endothelial cell (EC) marker (CD31) through triple immunohistochemistry and confirmed that both EndMT and EC proliferation contribute to atrial endocardial fibrosis during AF in TGF-β transgenic mice and AF patient tissue sections.
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