Daren Wang

TL;DR: In PH, miR-124 regulates the PKM2/PKM1 ratio, the overall metabolic, proliferative, and inflammatory state of cells, which may open unique therapeutic prospects in targeting the dynamic glycolytic and mitochondrial interactions and between mesenchymal inflammatory cells in PH.

TL;DR: Stable decreases in miR-124 expression contribute to an epigenetically reprogrammed, highly proliferative, migratory, and inflammatory phenotype of hypertensive pulmonary adventitial fibroblasts.

TL;DR: This study demonstrates for the first time that TLR2/NF-κB signaling mediates endothelial inflammation under high pulsatility flow caused by upstream stiffening, but the role of TLR4 in flow pulsatility-mediated endothelial mechanotransduction remains unclear.

TL;DR: In their letter, Bogaard et al appreciate that HDAC inhibitors “may mitigate pulmonary vascular remodeling through effects on lung endothelial cells or vascular smooth muscle cells” but are concerned about the possibility that “HDAC inhibitors threaten the heart’s adaptive response to pressure overload.