ArticleMolecular biology reports2026
Paraprobiotic Lactiplantibacillus plantarum MYO ameliorates dexamethasone-induced muscle atrophy: implications for age-related sarcopenia.
Article in Molecular biology reports, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSarcopenia, characterized by the progressive age-related decline in skeletal muscle mass, strength, and function, represents a major unmet need in geriatric health. Effective and safe interventions to prevent or ameliorate muscle atrophy are urgently required.
methodsThis study evaluated the effects of LPM2, a heat-killed paraprobiotic Lactiplantibacillus plantarum MYO isolated from Panax ginseng sprouts, using a dexamethasone (DEX)-induced mouse model of muscle atrophy that recapitulates key features of age-related sarcopenia.
resultsLPM2 administration significantly attenuated DEX-induced muscle wasting, preserving skeletal muscle mass and improving muscle performance. At the molecular level, LPM2 suppressed catabolic markers associated with muscle degradation, including Atrogin-1 and Myostatin, while restoring anabolic signaling pathways, particularly 4E-BP1. In addition, LPM2 exhibited a favorable safety profile, with no observable toxicity in major organs and beneficial effects on liver and kidney metabolic markers.
conclusionsThese findings demonstrate that LPM2 effectively modulates muscle protein turnover and protects against glucocorticoid-induced muscle atrophy. Given its paraprobiotic nature, ginseng-derived origin, and excellent safety profile, LPM2 represents a promising nutritional or therapeutic candidate for the prevention and management of age-related sarcopenia, supporting healthy aging and extended healthspan.
Indexed as
Identifiers
41746443What 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.