Evidence map›Paper›PMID 37812720›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

The metabolomic physics of complex diseases.

Shuang Wu, Xiang Liu, Ang Dong, Claudia Gragnoli, Christopher Griffin, Jie Wu, Shing-Tung Yau, Rongling Wu

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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. Graph statistics theory of individualized quantitative genetics under haplotype-resolved genome assembly.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. A Statistical Mechanics Model to Decode Tissue Crosstalk During Graft Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Hypernetwork modeling and topology of high-order interactions for complex systems.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. The metabolomic physics of complex diseases.Proceedings of the National Academy of Sciences of the United States of America · 2023
    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

8 authors.

Shuang WuCenter for Computational Biology, College of Biological Sciences and Technology, Beijing Forestry University, Beijing 100083, China.
Xiang LiuChern Institute of Mathematics, Nankai University, Tianjin 300071, China.
Ang DongCenter for Computational Biology, College of Biological Sciences and Technology, Beijing Forestry University, Beijing 100083, China.
Claudia GragnoliDepartment of Public Health Sciences, Penn State College of Medicine, Hershey, PA 17033.
Christopher GriffinApplied Research Laboratory, The Pennsylvania State University, University Park, PA 16802.ORCID 0000-0002-9962-9540
Jie WuBeijing Yanqi Lake Institute of Mathematical Sciences and Applications, Beijing 101408, China.
Shing-Tung YauBeijing Yanqi Lake Institute of Mathematical Sciences and Applications, Beijing 101408, China.ORCID 0000-0003-3394-2187
Rongling WuBeijing Yanqi Lake Institute of Mathematical Sciences and Applications, Beijing 101408, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human diseases involve metabolic alterations. Metabolomic profiles have served as a vital biomarker for the early identification of high-risk individuals and disease prevention. However, current approaches can only characterize individual key metabolites, without taking into account the reality that complex diseases are multifactorial, dynamic, heterogeneous, and interdependent. Here, we leverage a statistical physics model to combine all metabolites into bidirectional, signed, and weighted interaction networks and trace how the flow of information from one metabolite to the next causes changes in health state. Viewing a disease outcome as the consequence of complex interactions among its interconnected components (metabolites), we integrate concepts from ecosystem theory and evolutionary game theory to model how the health state-dependent alteration of a metabolite is shaped by its intrinsic properties and through extrinsic influences from its conspecifics. We code intrinsic contributions as nodes and extrinsic contributions as edges into quantitative networks and implement GLMY homology theory to analyze and interpret the topological change of health state from symbiosis to dysbiosis and vice versa. The application of this model to real data allows us to identify several hub metabolites and their interaction webs, which play a part in the formation of inflammatory bowel diseases. The findings by our model could provide important information on drug design to treat these diseases and beyond.

Indexed as

EcosystemMetabolomicsBiomarkersHumansModels, StatisticalPhysicsBiomarkersallometric scaling lawevolutionary game theoryidopNetworkmetabolic interactionquasi-dynamic ordinary differential equations

Identifiers

PMID37812720
PMCPMC10589719

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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 OpenQuestion graph.