Evidence map›Paper›PMID 39802611›Full record

ArticleToxicology research2025

Inorganic arsenic modulates cell apoptosis by regulating Argonaute 2 expression via the p53 pathway.

Kunyu Du, Jingkui Shu, Jintao Wu, Na Liu, He Ma, Jinyun Jiang, Yuefeng He, Xinan Wu

Abstract read
In one paragraph

Article in Toxicology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Kunyu DuYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
Jingkui ShuYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
Jintao WuThe 1st Affiliated Hospital of Kunming Medical University, No. 295 Xichang Road, Kunming, Yunnan 650032, China.
Na LiuYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
He MaYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
Jinyun JiangYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
Yuefeng HeYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.ORCID https://orcid.org/0000-0002-4604-8064
Xinan WuYunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study explores the role of Argonaute 2 (AGO2) in the induction of apoptosis by arsenic in 16HBE cells and investigates the association between AGO2 expression and arsenic exposure in a human population. By silencing AGO2 with siRNA, we examined its impact on cell viability and apoptosis using CCK-8, HO-PI, and JC-1 assays, complemented by qRT-PCR and Western blot analyses for gene and protein expressions. Our findings revealed a significant correlation between AGO2 expression and levels of exposure to inorganic arsenic (iAs), which was more pronounced than with other arsenic forms such as monomethylarsonic (MMA) and dimethylarsinic acids (DMA). The results showed that silencing AGO2 not only reduced cell viability but also intensified apoptosis, highlighting its role in activating the p53 pathway. This was further supported by increased phosphorylation of p53 at Ser392 and Thr55, reinforcing AGO2's involvement in apoptotic processes. The study underscores the potential of AGO2 as a therapeutic target in arsenic-related pathologies and highlights the critical need for managing occupational exposure to arsenic.

Indexed as

Argonaute 2 (AGO2)arsenic toxicologycell apoptosisinorganic arsenic(iAs)p53 pathway

Identifiers

PMID39802611
PMCPMC11711588

What OpenQuestion holds

Textmetadata
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.