二ホウ化マグネシウムナノシートによる肺動脈性肺高血圧症関連右心不全への効果：マルチオミクス解析によるフェロトーシス抑制機序の解明
Pulmonary arterial hypertension (PAH) is a progressive vascular disease marked by pathological remodeling, cellular proliferation, apoptosis resistance, inflammation, and fibrosis, ultimately leading to right heart failure (RHF). The right ventricle initially compensates through hypertrophy but eventually undergoes dilation, contractile dysfunction, and fibrosis. No clinically established interventions directly target right ventricular adaptation. Molecular hydrogen possesses antioxidative, anti-inflammatory, and anti-apoptotic properties, yet its application in PAH-associated RHF has not been explored, partly due to hydrogen's explosive risk and limited bioavailability. This study developed hydrogen-releasing magnesium diboride nanosheets (MBNs) and applied integrated transcriptomic and proteomic analyses to assess their cardioprotective effects in a PAH-induced RHF model. The LC3/ATG5/NCOA4/FTH1 axis was identified as a key pathway through which MBNs suppress ferroptosis, revealing a mechanistic basis for the observed cardiac protection.
MBNs modulate autophagy-dependent ferritin degradation (ferritinophagy) through the LC3/ATG5/NCOA4/FTH1 pathway, thereby suppressing ferroptosis and conferring right ventricular cardioprotection.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/41308938