Evidence map›Paper›PMID 37541252›Full record

ArticleCell reports. Medicine2023

Artificial cells delivering itaconic acid induce anti-inflammatory memory-like macrophages to reverse acute liver failure and prevent reinjury.

Na Yin, Wenjun Zhang, Xiao-Xin Sun, Runxiu Wei, Qiang Yang, Fengming He, Changrui Li, Ling Guo, Min Feng

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Leveraging Macrophage Metabolic Reprogramming for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Metabolic Messengers: itaconate.Nature metabolism · 2024
    Review
  12. 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 at 4 institutions in 2 countries.

Na YinSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China.
Wenjun ZhangSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China.
Xiao-Xin SunDepartment of Molecular & Medical Genetics, Oregon Health & Science University, Portland, OR 97239, USA.
Runxiu WeiSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China.
Qiang YangSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China.
Fengming HeSchool of Pharmaceutical Sciences, Xiamen University, South Xiang-An Road, Xiamen 361102, China.
Changrui LiGuangzhou Zhixin High School, Zhixin South Road, Guangzhou 510080, China.
Ling GuoSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China; Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China. Electronic address: guoling@hainanu.edu.cn.
Min FengSchool of Pharmaceutical Sciences, Sun Yat-Sen University, University Town, Guangzhou 510006, China. Electronic address: fengmin@mail.sysu.edu.cn.
Sun Yat-sen University · CNOregon Health & Science University · USShenzhen Baoan High School Group · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic macrophages represent a key cellular component of the liver and are essential for the progression of acute liver failure (ALF). We construct artificial apoptotic cells loaded with itaconic acid (AI-Cells), wherein the compositions of the synthetic plasma membrane and surface topology are rationally engineered. AI-Cells are predominantly localized to the liver and further transport to hepatic macrophages. Intravenous administration of AI-Cells modulates macrophage inflammation to protect the liver from acetaminophen-induced ALF. Mechanistically, AI-Cells act on caspase-1 to suppress NLRP3 inflammasome-mediated cleavage of pro-IL-1β into its active form in macrophages. Notably, AI-Cells specifically induce anti-inflammatory memory-like hepatic macrophages in ALF mice, which prevent constitutive overproduction of IL-1β when liver reinjury occurs. In light of AI-Cells' precise delivery and training of memory-like hepatic macrophages, they offer promising therapeutic potential in reversing ALF by finely controlling inflammatory responses and orchestrating liver homeostasis, which potentially affect the treatment of various types of liver failure.

Indexed as

Artificial CellsLiver Failure, AcuteReinjuriesAnimalsAnti-Inflammatory AgentsMacrophagesMiceSuccinatesAnti-Inflammatory Agentsitaconic acidSuccinatesacute liver failureartificial cellsIL-1βitaconic acidmemory-like hepatic macrophages

Identifiers

PMID37541252
PMCPMC10439255
OpenAlexW4385554206

What OpenQuestion 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 OpenQuestion graph.