ArticleAging medicine (Milton (N.S.W))2025
Mechanism of RNA Oxidation and Its Inhibitor Involved in Ang II-Induced Cardiomyocyte Hypertrophy.
Article in Aging medicine (Milton (N.S.W)), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To explore the mechanism of RNA oxidation and its inhibitor MTHI involved in cardiomyocyte hypertrophy. Methods: The hypertrophic H9c2 cardiomyocytes were stimulated with different concentrations and times of Ang II (Ang II) to construct a model of hypertensive heart failure in vitro. Transfection of H9c2 cells with the MTH1 overexpression plasmid was performed. The mRNA expression of ANP, BNP, and β-MHC in each experimental group was detected by PCR. The expression of 8-oxoG in H9c2 cells was determined by immunofluorescence and enzyme-linked immunosorbent assay (ELISA). The activation of the ERK-MAPK pathway and the amount of MTH1 protein were detected by WB semi-quantitative method. Results: Notably, RNA oxidation is a critical event in cellular senescence, and its accumulation is strongly linked to the aging process and the development of age-related diseases. In our model of cardiomyocyte hypertrophy, the oxidative damage of RNA was aggravated, and the expression of MTH1 was increased. At the same time, the sequence of ERK-MAPK pathway proteins was activated. It can be seen that the oxidative damage of RNA is related to the process of cardiomyocyte hypertrophy. After transfection of the MTH1 overexpression plasmid into the cardiomyocyte hypertrophy model, we found that the amount of 8-oxoG decreased, and the activation of ERK-MAPK signaling pathway proteins decreased, and H9c2 cell hypertrophy decreased. Therefore, we concluded that 8-oxoG may aggravate the hypertrophy of the cardiomyocyte hypertrophy model by activating the ERK-MAPK pathway. Conclusion: The oxidative damage of RNA is involved in the process of cardiomyocyte hypertrophy. The mechanism may be that 8-oxoG, a product of RNA oxidation, activates the downstream ERK-MAPK signaling pathway. These findings provide new perspectives for further exploration into the role of RNA oxidation in the pathogenesis of age-related diseases, particularly heart failure.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.