Evidence map›Paper›PMID 38879122›Full record

ArticleJournal of advanced research2025

Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.

Jingzeng Cai, Jiaqiang Huang, Di Li, Xintong Zhang, Bendong Shi, Qiaohan Liu, Cheng Fang, Shiwen Xu, Ziwei Zhang

Abstract read
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ROS: their roles in diminished ovarian reserve.Frontiers in endocrinology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Lycopene andPharmaceuticals (Basel, Switzerland) · 2024
    Article
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

9 authors.

Jingzeng CaiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Jiaqiang HuangBeijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing 100083, China.
Di LiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Xintong ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Bendong ShiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Qiaohan LiuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Cheng FangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Shiwen XuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, China. Electronic address: shiwenxu@neau.edu.cn.
Ziwei ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, China. Electronic address: zhangziwei@neau.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMetabolic inflammation (metaflammation) in obesity is primarily initiated by proinflammatory macrophage infiltration into adipose tissue. SelenoM contributes to the modulation of antioxidative stress and inflammation in multiple pathological processes; however, its roles in metaflammation and the proinflammatory macrophage (M1)-like state in adipose tissue have not been determined.

objectivesWe hypothesize that SelenoM could effectively regulate metaflammation via the Hippo-YAP/TAZ-ROS signaling axis in obesity derived from a high-fat diet.

methodsMorphological changes in adipose tissue were examined by hematoxylin-eosin (H&E) staining and fluorescence microscopy. The glucose tolerance test (GTT) and insulin tolerance test (ITT) were used to evaluate the impact of SelenoM deficiency on blood glucose levels. RNA-Seq analysis, LC-MS analysis, Mass spectrometry analysis and western blotting were performed to detect the levels of genes and proteins related to glycolipid metabolism in adipose tissue.

resultsHerein, we evaluated the inflammatory features and metabolic microenvironment of mice with SelenoM-deficient adipose tissues by multi-omics analyses. The deletion of SelenoM resulted in glycolipid metabolic disturbances and insulin resistance, thereby accelerating weight gain, adiposity, and hyperglycemia. Mice lacking SelenoM in white adipocytes developed severe adipocyte hypertrophy via impaired lipolysis. SelenoM deficiency aggravated the generation of ROS by reducing equivalents (NADPH and glutathione) in adipocytes, thereby promoting inflammatory cytokine production and the M1-proinflammatory reaction, which was related to a change in nuclear factor kappa-B (NF-κB) levels in macrophages. Mechanistically, SelenoM deficiency promoted metaflammation via Hippo-YAP/TAZ-ROS-mediated transcriptional regulation by targeting large tumor suppressor 2 (LATS2). Moreover, supplementation with N-acetyl cysteine (NAC) to reduce excessive oxidative stress partially rescued adipocyte inflammatory responses and macrophage M1 activation.

conclusionOur data indicate that SelenoM ameliorates metaflammation mainly via the Hippo-YAP/TAZ-ROS signaling axis in obesity. The identification of SelenoM as a key regulator of metaflammation presents opportunities for the development of novel therapeutic interventions targeting adipose tissue dysfunction in obesity.

Indexed as

Adaptor Proteins, Signal TransducingInflammationObesityReactive Oxygen SpeciesTranscription FactorsAdipose TissueAnimalsDiet, High-FatHippo Signaling PathwayMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesSignal TransductionAdaptor Proteins, Signal TransducingProtein Serine-Threonine KinasesReactive Oxygen SpeciesTranscription FactorsYap1 protein, mouseYAP-Signaling ProteinsHippo-YAP/TAZ-ROSMetaflammationObesityOxidative stressSelenoM

Identifiers

PMID38879122
PMCPMC12126717

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.