ArticleInternational journal of molecular medicine2026
IDH2 lactylation regulates mitochondrial dysfunction injury induced by myocardial ischemia‑reperfusion via the AMPK signaling pathway.
Article in International journal of molecular medicine, 2026. 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic cardiomyopathy ranks as a principal cause of death and incapacity worldwide. Myocardial ischemia‑reperfusion injury (MIRI) caused by percutaneous coronary intervention is a major threat in the treatment of ischemic cardiomyopathy. Although lactylation (Kla) is extensively implicated in numerous pathological processes, its role and specific effects in MIRI remain unclear. Lactylation proteomics was used to identify proteins with different modifications during ischemia‑reperfusion injury. Co‑immunoprecipitation experiments were utilized to detect isocitrate dehydrogenase 2 (IDH2) lactylation levels. Immuno-fluorescence staining was applied to confirm intracellular lactylation levels. TUNEL, DHE and MitoSOX staining were used to measure oxidative damage in cells and tissues. An oxygen consumption rate experiment and the ATP assay were conducted to determine mitochondrial function. Western blots were utilized to detect changes in proteins related to mitochondrial functional homeostasis and downstream signal alterations. Excessive lactate accumulation was observed in MIRI model mice. This accumulation exacerbated the decline in cardiac function and the damage to cardiomyocytes in mice after MIRI. The lactylation of IDH2 in mitochondria was found to play a regulatory role in mitochondrial dysfunction and MIRI. Regarding the mechanism, it was verified that high IDH2 K275 lactylation caused a reduction in its enzymatic activity and decreased the production of α‑ketoglutarate in the tricarboxylic acid cycle. Consequently, the activation of the AMPK pathway was inhibited, and mitochondrial damage and functional impairment were aggravated. It was also found that SIRT3 regulated and prevented IDH2 lactylation. The results of the present study indicated that IDH2 lactylation, which is elevated due to lactate accumulation and negatively regulated by SIRT3, contributes to the exacerbation of MIRI by regulating the functional homeostasis of mitochondria. This discovery offers a new therapeutic concept and target for MIRI prevention.
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.