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ferroptosis, pubmed, group, article, cell, fer, google, scholar, pulmonary, rats, cas, hmgb, nlrp, inflammasome, mctinduced, paecs, tlr, mct, cells, hypertension, sham, central, lung, expression, death, model, endothelial, versus, vascular, groups, inflammation, protein, macrophages, study, data, paec, inflammatory, nature, progression, treatment, mitochondrial, involved, fig, levels, analysis, role, iron, fth, nox, china,

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nature portfolio ovarian research privacy policy nature 447 nature advertising nf-kappab signaling pathways α-smooth muscle actin rage/nfkappab signaling pathways reprints hypoxia-induced mitogenic factor rhoa/rho kinase signaling monocrotaline-induced pulmonary hypertension hypoxia-induced pulmonary hypertension abnormal ferroptosis-related proteins pilocarpine-induced epileptic seizures nlrp3 inflammasome-related proteins hmgb1/tlr4/nlrp3 inflammasome signalling full size image enzyme-linked immunosorbent assay uvb-induced skin inflammation64 author information authors increased ferroptosis-dependent cytotoxicity iron-dependent lipid peroxidation tumour necrosis factor-α ice-cold ripa buffer improves long-term outcomes elisa kits radiation-induced lung fibrosis acetylated low-density lipoprotein jia-quan li inflammation-related disease processes7 mct-induced paecs derived exert anti-inflammatory effects permissions saline + vehicle-treated control group trigger inflammatory responses mct + fer-1 pretreatment groups author correspondence original author p53 inhibits ferroptosis cell volume shrinkage mct-induced ph rats bar graph showing pulmonary arterial hypertension pulmonary vascular remodelling ferroptosis-related proteins rabbit anti-α-sma article xie mct-induced rats compared

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• Fifty years of monocrotaline-induced pulmonary hypertension: What Has It Meant to the Field?

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         headline:Endothelial cell ferroptosis mediates monocrotaline-induced pulmonary hypertension in rats by modulating NLRP3 inflammasome activation
         description:Inflammation triggers pulmonary vascular remodelling. Ferroptosis, a nonapoptotic form of cell death that is triggered by iron-dependent lipid peroxidation and contributes to the pathogenesis of several inflammation-related diseases, but its role in pulmonary hypertension (PH) has not been studied. We examined endothelial cell ferroptosis in PH and the potential mechanisms. Pulmonary artery endothelial cells (PAECs) and lung tissues from monocrotaline (MCT)-induced PH rats were analysed for ferroptosis markers, including lipid peroxidation, the labile iron pool (LIP) and the protein expression of glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1) and NADPH oxidase-4 (NOX4). The effects of the ferroptosis inhibitor ferrostatin-1 (Fer-1) on endothelial cell ferroptosis and pulmonary vascular remodelling in MCT-induced rats were studied in vitro and in vivo. Ferroptosis was observed in PAECs from MCT-induced PH rats in vitro and in vivo and was characterized by a decline in cell viability accompanied by increases in the LIP and lipid peroxidation, the downregulation of GPX4 and FTH1 expression and the upregulation of NOX4 expression. High-mobility group box 1 (HMGB1)/Toll-like receptor 4 (TLR4)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signalling was measured by western blotting. These changes were significantly blocked by Fer-1 administration in vitro and in vivo. These results suggest that Fer-1 plays a role in inhibiting ferroptosis-mediated PAEC loss during the progression of PH. The ferroptosis-induced inflammatory response depended on the activation of HMGB1/TLR4 signalling, which activated the NLRP3 inflammasome in vivo. We are the first to suggest that pulmonary artery endothelial ferroptosis triggers inflammatory responses via the HMGB1/TLR4/NLRP3 inflammasome signalling pathway in MCT-induced rats. Treating PH with a ferroptosis inhibitor and exploring new treatments based on ferroptosis regulation might be promising therapeutic strategies for PH.
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      headline:Endothelial cell ferroptosis mediates monocrotaline-induced pulmonary hypertension in rats by modulating NLRP3 inflammasome activation
      description:Inflammation triggers pulmonary vascular remodelling. Ferroptosis, a nonapoptotic form of cell death that is triggered by iron-dependent lipid peroxidation and contributes to the pathogenesis of several inflammation-related diseases, but its role in pulmonary hypertension (PH) has not been studied. We examined endothelial cell ferroptosis in PH and the potential mechanisms. Pulmonary artery endothelial cells (PAECs) and lung tissues from monocrotaline (MCT)-induced PH rats were analysed for ferroptosis markers, including lipid peroxidation, the labile iron pool (LIP) and the protein expression of glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1) and NADPH oxidase-4 (NOX4). The effects of the ferroptosis inhibitor ferrostatin-1 (Fer-1) on endothelial cell ferroptosis and pulmonary vascular remodelling in MCT-induced rats were studied in vitro and in vivo. Ferroptosis was observed in PAECs from MCT-induced PH rats in vitro and in vivo and was characterized by a decline in cell viability accompanied by increases in the LIP and lipid peroxidation, the downregulation of GPX4 and FTH1 expression and the upregulation of NOX4 expression. High-mobility group box 1 (HMGB1)/Toll-like receptor 4 (TLR4)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signalling was measured by western blotting. These changes were significantly blocked by Fer-1 administration in vitro and in vivo. These results suggest that Fer-1 plays a role in inhibiting ferroptosis-mediated PAEC loss during the progression of PH. The ferroptosis-induced inflammatory response depended on the activation of HMGB1/TLR4 signalling, which activated the NLRP3 inflammasome in vivo. We are the first to suggest that pulmonary artery endothelial ferroptosis triggers inflammatory responses via the HMGB1/TLR4/NLRP3 inflammasome signalling pathway in MCT-induced rats. Treating PH with a ferroptosis inhibitor and exploring new treatments based on ferroptosis regulation might be promising therapeutic strategies for PH.
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