How Hydrogen Therapy May Help Treat Deadly Lung Condition ARDS

Authors
Journal
Frontiers in Immunology
Year
DOI
10.3389/fimmu.2026.1899718
Study Type
clinical
Peer Reviewed
Yes
Country
China
Health Condition
Acute Respiratory Distress Syndrome (ARDS)
Body System
Respiratory

TL;DR

When someone gets a severe lung condition called ARDS, their cells' tiny power generators (mitochondria) break down and stop working right, which makes the lungs even more damaged. Scientists are finding new ways to fix these power generators with special medicines, which could lead to better treatments for this deadly condition.

Key Finding

Mitochondrial dysfunction drives a damaging cycle of inflammation and abnormal energy metabolism in ARDS, and hydrogen is mentioned among several experimental agents that may help restore normal mitochondrial function in preclinical (lab or animal) models.

Summary

This is a review article — not a new experiment — that summarizes existing research on why mitochondria (the energy-producing parts of cells) malfunction in acute respiratory distress syndrome (ARDS), a severe and often fatal lung condition. The authors explain how damaged mitochondria trigger inflammation and cause cells to shift to a less efficient energy process, making lung injury worse. They also survey potential treatments, briefly mentioning hydrogen among several experimental approaches that have shown promise in lab and animal studies. No new data was collected or tested in this paper.

Practical Takeaway

This review suggests that hydrogen may play a role in supporting mitochondrial health during severe lung injury, but it is cited only briefly alongside many other experimental compounds. Because this is a review of preclinical research — not a human clinical trial — no conclusions about hydrogen water's effectiveness in people with ARDS can be drawn from it.

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening condition with high mortality and limited effective pharmacotherapies. Accumulating evidence has established mitochondrial dysfunction as a central pathogenic hub in ARDS. Injured mitochondria exhibit excessive reactive oxygen species production, impaired mitophagy, aberrant dynamics (predominantly Drp1-mediated fission), reduced biogenesis, and release of mitochondrial DNA as a damage-associated molecular pattern. These alterations trigger inflammatory cascades via the cGAS/STING and NLRP3 pathways, while simultaneously driving a metabolic shift from oxidative phosphorylation to aerobic glycolysis, the Warburg effect. Key glycolytic enzymes, including PKM2, PDK4, GAPDH, and PGK1, reinforce mitochondrial damage through lactate production and HIF-1α stabilization, creating a vicious cycle. Notably, PFKFB3 exhibits cell-type-specific duality, exerting protective effects in alveolar epithelial cells while promoting NETosis in neutrophils. Distinct cell types in the lung, alveolar macrophages, neutrophils, alveolar epithelial cells, and pulmonary endothelial cells exhibit unique mitochondrial and metabolic alterations that collectively perpetuate injury and impair repair. Therapeutically, mitochondria-targeted agents (MitoQ, MOTS-c), modulators of mitochondrial dynamics (baicalein, hydrogen), inhibitors of glycolytic enzymes (PFKFB3, PKM2, PDK4), natural compounds (1-octyl itaconate, shikonin, scutellarin), and mesenchymal stromal cell-mediated mitochondrial transfer have shown promise in preclinical models. This review synthesizes current understanding of the regulatory mechanisms linking mitochondrial dysfunction and metabolic reprogramming in ARDS, discusses cell-type-specific contributions, and highlights emerging therapeutic strategies. Targeting mitochondrial homeostasis and the associated glycolytic shift may offer a transformative approach to ARDS treatment, though challenges related to cell specificity, safety, and clinical translation remain.