Evidence map›Paper›PMID 37164984›Full record

ReviewCell death discovery2023

Serum amyloid protein A in inflammatory bowel disease: from bench to bedside.

Rirong Chen, Qia Chen, Jieqi Zheng, Zhirong Zeng, Minhu Chen, Li Li, Shenghong Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
16.5field-weighted citation impact, top 1% of its field
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

39 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
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  12. Divergent T Cell Phenotypes Define Pediatric Crohn's Disease and Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025
    Article
  13. Article
  14. Mitigation ofMicrobiology spectrum · 2025
    Article
  15. Lymphocyte Fractions as Indicators of T-Helper 1/T-Helper 2 Cytokine Profiles in Inflammatory Bowel Disease.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Article
  16. Article
  17. Circulation. Heart failure · 2025
    Article
  18. Article
  19. Article
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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

7 authors at 1 institution in 1 country.

Rirong Chen *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID http://orcid.org/0000-0002-8230-1995
Qia Chen *Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Jieqi ZhengDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Zhirong ZengDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Minhu ChenDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Li LiDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. lili333@mail2.sysu.edu.cn.
Shenghong ZhangDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. zhshh3@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-9088-8781
Sun Yat-sen University · CN

Funding

Guangdong Science and Technology Department (Science and Technology Department, Guangdong Province) #2021A1515220107National Natural Science Foundation of China (National Science Foundation of China) #82270555, #82070538, #81870374
6 · The paper itself

Abstract

Inflammatory bowel diseases (IBD) is featured by gastrointestinal inflammation and a disease course with alternating recurrence and remission. The global burden caused by IBD has significantly boosted in recent years, necessitating treatment optimization. Serum amyloid A (SAA) is a class of 104 amino acid conservative acute-phase proteins, which is essential in immune-mediated inflammatory processes, like IBD. The SAA monomeric structure is composed of four α-helical regions and a C-terminal amorphous tail. Its disordered structure enables multiple bindings to different ligands and permits multiple functions. It has been proven that SAA has dual roles in the inflammatory process. SAA stimulates the pro-inflammatory cytokine expression and promotes the pathogenic differentiation of TH17 cells. In addition, SAA can remove toxic lipids produced during inflammatory responses and membrane debris from dead cells, redirect HDL, and recycle cholesterol for tissue repair. In IBD, SAA acts on gut epithelium barriers, induces T-cell differentiation, and promotes phagocytosis of Gram-negative bacteria. Owing to the tight connection between SAA and IBD, several clinical studies have taken SAA for a biomarker for diagnosis, assessing disease activity, and predicting prognosis in IBD. Furthermore, 5-MER peptide, a drug specifically targeting SAA, has shown anti-inflammatory effects in some SAA-dependent animal models, providing novel insights into the therapeutic targets of IBD.

Identifiers

PMID37164984
PMCPMC10172326
OpenAlexW4376114102

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.