Evidence map›Paper›PMID 36015636›Full record

ArticlePolymers2022

Cytotoxicity and Apoptotic Mechanism of 2-Hydroxyethyl Methacrylate via Genotoxicity and the Mitochondrial-Dependent Intrinsic Caspase Pathway and Intracellular Reactive Oxygen Species Accumulation in Macrophages.

Chien-Ying Lee, Yung-Chuan Ho, Shiuan-Shinn Lee, Yi-Ching Li, Mei-Yu Lai, Yu-Hsiang Kuan

Open access · goldAbstract read
In one paragraph

Article in Polymers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Evolution of Dental Resin Adhesives-A Comprehensive Review.Journal of functional biomaterials · 2025
    Review
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

6 authors at 2 institutions in 1 country.

Chien-Ying LeeDepartment of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0001-8159-4645
Yung-Chuan HoSchool of Medical Applied Chemistry, Chung Shan Medical University, Taichung 40201, Taiwan.
Shiuan-Shinn LeeSchool of Public Health, Chung Shan Medical University, Taichung 40201, Taiwan.
Yi-Ching LiDepartment of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Mei-Yu LaiDepartment of Nursing, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.
Yu-Hsiang KuanDepartment of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0002-8991-6394
Chung Shan Medical University Hospital · TWChung Shan Medical University · TW

Funding

Chung Shan Medical University Hospital research program of Taiwan CSH-2020-C-006Ministry of Science and Technology of Taiwan MOST 109-2320-B-040-MY3
6 · The paper itself

Abstract

Macrophages are mainly active cells of the immune system and play a role in the defense of pathogens. However, the overactivation of macrophages by fatal pathogens can result in toxic responses. 2-hydroxyethyl methacrylate (HEMA), which is a hydrophilic monomer, is used in dental adhesive reagents and composite resins as well as biocompatible hydrogels. The mechanisms underlying the genotoxicity engendered by HEMA-induced apoptosis that leads to cytotoxicity remain unclear. Accordingly, this study was conducted to clarify such mechanisms. The results showed that HEMA induced cell toxicity in RAW264.7 macrophages depending on the concentration. A higher HEMA concentration was associated with a higher level of apoptosis and genotoxicity. Moreover, HEMA induced a concentration-dependent increase in mitochondrial dysfunction and the intrinsic caspase pathway, including the activation of caspase-3 and caspase-9. HEMA was also found to upregulate intracellular reactive oxygen species generation and to decrease the activity of antioxidant enzymes, including superoxide dismutase and catalase. Taken together, the mitochondrial-dependent intrinsic caspase pathway and intracellular reactive oxygen species accumulation were found to mediate HEMA-induced genotoxicity and apoptosis, leading to cytotoxicity in RAW264.7 macrophages.

Indexed as

apoptosiscaspasescytotoxicitygenotoxicityHEMARAW264.7 macrophages

Identifiers

PMID36015636
PMCPMC9412604
OpenAlexW4293511108

What OpenQuestion holds

Textmetadata
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.