Observational studyMedicine2025
TWEAK/Fn14 hypomethylation and higher plasma TWEAK and TNF-α levels are related to sarcopenic obesity in community-dwelling elderly in Xinjiang.
Observational study in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Inhibition of TWEAK/Fn14 Ameliorates Sarcopenic Obesity by Restoring Mitochondrial Biogenesis via the AMPK/SIRT1/PGC-1α Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
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
Sarcopenic obesity is a primary factor contributing to the decline in the quality of life among the elderly in our country. Studies have shown that hypomethylation of tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) is associated with sarcopenia. Our research primarily explores whether this mechanism also affects the progression of sarcopenic obesity. A total of 120 subjects were grouped into the case (sarcopenic obesity) and control (non-sarcopenic and nonobese) groups, with 60 subjects in each group based on power test (medium effect size, power = 80%). Bisulfite sequencing was used to assess the methylation status of TWEAK/Fn14 in these subjects. ELISA was employed to measure the plasma concentrations of TWEAK, tumour necrosis factor-alpha (TNF-α), interleukin (IL)-4, IL-6, and IL-10. SPSS 17.0 and R software was used for statistical analysis, employing multiple logistic regression to adjust for residual confounding factors, and Student t tests for difference analysis. Compared to the case group, the control group had higher methylation levels at CpG20, CpG30 sites in TWEAK (P = .043 for both). Additionally, the control group showed higher methylation level at CpG25 site in Fn14 (P = .025). After adjusting for hypertension, diabetes, triglyceride levels, gender, and age, Student t tests covariance confirmed significant differences in the enrichment levels of TWEAK, TNF-α, IL-10, and IL-4 of patients in case group (PTWEAK = .017, PTNF-α < .001, PIL-10 = .010, PIL-4 = .016). Multivariate logistic regression analysis revealed that higher plasma levels of TWEAK and TNF-α were significantly associated with the incidence of sarcopenic obesity (odds ratios = 1.024, 95% confidence interval = 1.006-1.042; odds ratios = 2.537, 95% confidence interval = 1.697-3.793). This evidence suggested that hypomethylation of TWEAK/Fn14 also affected sarcopenic obesity progression. Increased enrichment of TWEAK and TNF-α in plasma, along with hypomethylation of TWEAK and Fn14, promotes the occurrence of sarcopenic obesity may affect occurrence of sarcopenic obesity.
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.