ArticleFrontiers in pharmacology2025
Levocarnitine improves cardiac energy metabolic remodeling in myocarditis mice.
Article in Frontiers in pharmacology, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Energy metabolic remodeling represents a critical pathological mechanism in myocarditis progression. Levocarnitine (LC), an essential cofactor for fatty acid oxidation, demonstrates potential in modulating cardiac metabolism. This study investigated the therapeutic effects of LC on myocardial energy metabolic remodeling and explored the underlying molecular mechanisms. Methods: The experimental autoimmune myocarditis (EAM) mouse model was constructed using α-myosin. Cardiac function, myocardial inflammatory infiltration, and mitochondrial structure were evaluated using echocardiography, HE staining, and transmission electron microscopy, respectively. Metabolic parameters including free fatty acid (FFA), lactic acid (LAC), mitochondrial complex IV (COX IV) activity, and adenosine triphosphate (ATP) levels were measured using colorimetry. Serum heart-type fatty acid-binding protein (H-FABP) levels were measured by ELISA, and reactive oxygen species (ROS) levels were determined by flow cytometry. The expression of organic carnitine transporter type 2 (OCTN-2) and carnitine palmitoyltransferase-1B (CPT-1B) were determined by Western blot. Furthermore, network pharmacology and molecular docking were employed to predict the therapeutic targets and mechanisms of LC in myocarditis. The activity of the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) pathway and the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) were verified by Western blot. Results: LC treatment significantly improved cardiac function and attenuated myocardial inflammatory infiltration in EAM mice. It ameliorated mitochondrial structural damage, enhanced COX IV activity and ATP production, and reduced the accumulation of FFA, LAC and ROS in myocardial tissues. It also lowered serum H-FABP levels while upregulating the expression of OCTN-2 and CPT-1B. Combining network pharmacology and molecular docking, Akt was identified as the key therapeutic target of LC in cardiomyopathy and demonstrated good binding affinity with LC. Conclusion: LC effectively improved myocardial metabolic remodeling and alleviated cardiac insufficiency in myocarditis. The underlying mechanism may involve LC-mediated suppression of the PI3K/Akt signaling pathway, potentially linked to increased expression of the key mitochondrial regulator PGC-1α.
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.