Molecular hydrogen promotes retinal vascular regeneration and attenuates neovascularization and neuroglial dysfunction in oxygen-induced retinopathy mice.
Yatu Guo, Jiahui Qin, Ruiqiang Sun, Peng Hao, Zhixin Jiang, Yuchuan Wang, Zhiqi Gao, Huan Zhang, Keliang Xie, Wei Zhang · Biological research · 2024
Research-use notice
Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In mice, H₂ prevents the decreased density and reverses the morphologic and functional changes in retinal astrocytes caused by oxygen-induced injury. The authors linked these findings to activation of the Nrf2-Notch axis and HIF-1α/VEGF pathways. These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential for retinopathy and the biological pathways measured in this model.
What the Findings Mean
H2HUBB reviewed how inhaled hydrogen gas affected the outcomes measured in mice. H₂ prevents the decreased density and reverses the morphologic and functional changes in retinal astrocytes caused by oxygen-induced injury.
What the Researchers Studied
The researchers studied mice. The study used a preclinical animal experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
Source-reported hydrogen concentration: 4% source-reported H₂ gas concentration; Source-reported hydrogen exposure: 4% source-reported H₂ gas concentration; reported treatment duration: 5 days. H₂ prevents the decreased density and reverses the morphologic and functional changes in retinal astrocytes caused by oxygen-induced injury. The authors concluded that H₂ could be a promising therapeutic agent for ROP treatment and that its beneficial effect in human ROP might involve the activation of the Nrf2-Notch axis as well as HIF-1α/VEGF pathways. H₂ promotes the proliferation of HUVECs under hypoxia by negatively regulating the Dll4/Notch pathway and reducing ROS levels through Nrf2 pathway aligning with the findings in vivo.Moreover, the retinal oxygen-sensing mechanisms (HIF-1α/VEGF) are also involved in hydrogen-mediated retinal revascularization and neovascularization suppression. Hydrogen (H₂) is widely considered as a useful neuroprotective and antioxidative therapeutic method for hypoxic-ischemic disease without toxic effects. The authors linked these findings to activation of the Nrf2-Notch axis and HIF-1α/VEGF pathways.
Why These Findings Matter
These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential for retinopathy and the biological pathways measured in this model.
How Strong Is This Evidence?
This is preclinical animal evidence from a preclinical animal experiment. It is most informative for the disease model, mechanisms, biomarkers, and outcomes directly measured in the study.
Technical Study Details
H2HUBB classifies this publication as animal study with preclinical animal evidence. The research population or model was mice. The study used a preclinical animal experiment. The hydrogen delivery method was inhaled hydrogen gas. The source-reported hydrogen concentration was 4% source-reported H₂ gas concentration. The reported treatment duration was 5 days.
Limitations and Safety
Safety information: In addition, because of safety and clinical application considerations, the researchers choose the concentration of H₂ gas 3 ~ 4%, which was the safety concentration under the explosive concentration of H₂ gas in the mixture of H₂ gas and air as 4–75% [ 31 ].
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.