Hydrogen alleviates cardiac ferroptosis damage under chronic intermittent hypoxia conditions by targeting Nrf2.
Ji-Xian Song, Hong-Yu Han, Qing-Qing Liu, Meng-Fan Sun, Bo-Han Yu, Ya-Shuo Zhao, Ya-Jing Guo, En-Sheng Ji · International immunopharmacology · 2026
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 In vivo and in vitro CIH models were established to observe changes in cardiac function and pathological damage, hydrogen has been observed to reduce ferroptosis in H9C2 cells induced by RSL3, with effects comparable to those of Mito Q, Fer-1, and the Nrf2 activator SA. The authors concluded that these findings suggested that hydrogen could promote autophagy and reduce oxidative stress by activating the Nrf2 protein, thereby inhibiting ferroptosis and alleviating cardiac damage caused by CIH. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen affected the outcomes measured in In vivo and in vitro CIH models were established to observe changes in cardiac function and pathological damage. Hydrogen has been observed to reduce ferroptosis in H9C2 cells induced by RSL3, with effects comparable to those of Mito Q, Fer-1, and the Nrf2 activator SA.
What the Researchers Studied
The researchers studied In vivo and in vitro CIH models were established to observe changes in cardiac function and pathological damage. The study used a in vitro cell-culture laboratory experiment.
What Effects Did Molecular Hydrogen Have?
Hydrogen has been observed to reduce ferroptosis in H9C2 cells induced by RSL3, with effects comparable to those of Mito Q, Fer-1, and the Nrf2 activator SA. The authors concluded that these findings suggested that hydrogen could promote autophagy and reduce oxidative stress by activating the Nrf2 protein, thereby inhibiting ferroptosis and alleviating cardiac damage caused by CIH. Hydrogen could mitigate cardiac injury and ferroptosis induced by CIH, primarily through its sustained modulation of oxidative stress and the activation of autophagy.
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was In vivo and in vitro CIH models were established to observe changes in cardiac function and pathological damage. The study used a in vitro cell-culture laboratory experiment.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.