06/12/2025
Big News: A Major Breakthrough in Hydrogen Science
Fresh off the press this week!
Just-released paper in Redox Biology (5-Year IF 13.1, SCImago Q1) is a milestone for the entire hydrogen field.
For years, researchers and many of you have asked fundamental questions:
How does H2 work?
What does it actually bind to?
Why do its effects last long after the gas is gone?
How does it benefit the mitochondria?
And so on…
This publication provides a major part of the answer.
Read the press release: https://molecularhydrogeninstitute.org/study-identifies-first-molecular-target-of-hydrogen/
Read the published paper here:
https://www.sciencedirect.com/science/article/pii/S2213231725004653?via%3Dihub
What the Study Found
The study discovered that exposure to molecular hydrogen targets the Rieske iron-sulfur protein (RISP), triggering its LONP1-mediated degradation RISP is a critical component of mitochondrial Complex III. Hydrogen suppresses Complex III activity within minutes, signaling the cell that something has changed. This triggers a controlled mitochondrial hormetic response, a repair-and-strengthen cycle that mitochondria naturally use to stay resilient.
The cell responds by rebuilding and upregulating RISP, restoring and even enhancing function within hours.
This mechanism neatly explains many of the “paradoxical” findings in hydrogen research why some markers go up, others go down, yet outcomes typically improve.
This is an elegant unifying mechanism, indicating hydrogen is not biologically inert but like other small biological gases (NO⋅, CO, H₂S) but with its own unique twist.
This paper:
Further moves the field beyond the old “antioxidant” narrative
Shows that hydrogen interacts with a conserved mitochondrial protein
Helps explain the diverse and long-lasting effects seen across preclinical and clinical studies
This is the kind of work that shifts an entire field forward.
A groundbreaking paper published this week in Redox Biology reveals the first clearly defined molecular target of molecular hydrogen (H₂).