Evidence map›Paper›PMID 42063335›Full record

ArticleJournal of cachexia, sarcopenia and muscle2026

Elevated Circulating Ceramides 18:0 and 24:1 as a Risk Factor for Sarcopenia: In Vitro, Animal, and Clinical Evidence.

So Jeong Park, Ji Yeon Baek, Shibo Wei, Jin Young Lee, Yuna Lee, Sang-Hoon Lee, Il-Young Jang, Hyuk Sakong, Hyun Ju Yoo, Hee-Won Jung and 6 more

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In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

So Jeong ParkAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Ji Yeon BaekDivision of Geriatrics, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Shibo WeiDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Jin Young LeeAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Yuna LeeAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Sang-Hoon LeeAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Il-Young JangDivision of Geriatrics, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Hyuk SakongAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Hyun Ju YooDepartment of Convergence Medicine, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Hee-Won JungDivision of Geriatrics, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Eunju LeeDivision of Geriatrics, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Su Jung KimDepartment of Convergence Medicine, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Yunju JoDepartment of Microbiology, Wonkwang University School of Medicine, Iksan, South Korea.
Kyunggon KimDepartment of Digital Medicine, BK21 Project, University of Ulsan College of Medicine, Seoul, South Korea.
Dongryeol RyuDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Beom-Jun KimDivision of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.ORCID 0000-0001-8591-1759

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCeramides have garnered considerable attention as pro-aging bioactive lipids implicated in both metabolic dysfunction and musculoskeletal decline. Among these, C18:0 and C24:1 ceramides may play a role in the pathophysiology of sarcopenia, a key manifestation of age-related deterioration. However, their specific contributions to muscle degeneration remain poorly defined.

methodsC2C12 myoblasts and primary myoblasts were treated with C18:0 or C24:1 ceramides during differentiation to assess myotube formation, migration and intracellular reactive oxygen species (ROS) levels. Three-month-old C57BL/6 mice received daily intraperitoneal injections of C18:0 or C24:1 ceramides for 4 weeks to evaluate muscle morphology and function. In a human cohort of 165 community-dwelling older adults (≥ 65 years), serum ceramide levels were measured via LC-MS/MS and analysed in relation to sarcopenia parameters.

resultsBoth C18:0 and C24:1 ceramides significantly impaired myogenic differentiation in vitro, as evidenced by reduced myotube number, total myotube area, average area per myotube, nuclei count per myotube and fusion index, through ROS-mediated mechanisms (with up to an 8.6-fold increase in ROS production). Consistently, C18:0 and C24:1 ceramides markedly downregulated key myogenic markers and inhibited ITGB1-FAK-AKT signalling while promoting nuclear activation of FoxO-associated catabolic pathways. These deleterious effects were attenuated by treatment with the antioxidant N-acetylcysteine. In mice, systemic administration of either ceramide resulted in reduced muscle fibre cross-sectional area in the tibialis anterior (by 20.5% and 20.9% for C18:0 and C24:1, respectively) and soleus muscles (by 18.1% and 16.1%), accompanied by decreased grip strength, shorter grid hanging times and reduced latency to fall in the rotarod test. Clinically, in a cohort of 165 older adults (80.6% female; mean age 75.2 ± 5.2 years in controls and 79.7 ± 4.8 years in the sarcopenia group), serum levels of C18:0 and C24:1 ceramides were 27% and 14% higher, respectively, in individuals with sarcopenia compared to controls (p = 0.001 and 0.018). Furthermore, each standard deviation increase in serum C18:0 and C24:1 ceramide levels was associated with a 2.0- and 1.6-fold increased risk of sarcopenia, respectively (p = 0.003 and 0.040).

conclusionsOur findings reveal that circulating C18:0 and C24:1 ceramides are significantly associated with sarcopenia in older adults, while experimental models demonstrate they promote muscle atrophy through oxidative stress-induced impairment of myogenesis and muscle function. These ceramides may serve as minimally invasive biomarkers and potential therapeutic targets for age-related muscle decline. Interventions aimed at modulating ceramide metabolism could offer new avenues for sarcopenia prevention and treatment in aging populations.

Indexed as

CeramidesSarcopeniaAgedAged, 80 and overAnimalsBiomarkersCell DifferentiationDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLReactive Oxygen SpeciesRisk FactorsBiomarkersCeramidesReactive Oxygen Speciesbiomarkerceramidesoxidative stresssarcopeniatherapeutic target

Identifiers

PMID42063335
PMCPMC13133597

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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.