ArticleMedical gas research2026
Mitochondrial protection role of oxidoreductase-like domain containing 1 in myocardial cells under hypoxia.
Article in Medical gas research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mitochondria and related proteins are essential for mitochondrial preservation, the functions of some of these proteins remain unknown. The novel protein oxidoreductase-like domain containing 1 (OXLD1/C17orf90, UniProtKB Q5BKU9) have attracted our attention because of its correlation with mitochondria. This study revealed a decrease in OXLD1 levels in cardiomyocytes cultured in 1% oxygen for 24 hours. Suppressing OXLD1 increases mitochondrial injury under both normoxic and hypoxic conditions. This is evidenced by decreased mitochondrial membrane potential and increased reactive oxygen species production. Meanwhile, suppressing OXLD1 decreased mitochondrial oxidative phosphorylation. Overexpression of OXLD1 decreased mitochondrial injury under normoxia and hypoxia, as indicated by an increase in the mitochondrial membrane potential and a decrease in reactive oxygen species production. Moreover, overexpression of OXLD1 enhanced mitochondrial oxidative phosphorylation. Additionally, we found that OXLD1 regulates mitochondrial oxidative phosphorylation by affecting mitochondrial complexes I and V. OXLD1 plays a crucial role in protecting cardiomyocytes by improving mitochondrial function under low-oxygen conditions. OXLD1 achieves this protection through interactions with mitochondrial complexes I and V. Therefore, OXLD1 may serve as a new and important regulator of mitochondrial function.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.