SynthesisEnvironmental geochemistry and health2021
Relationship between p38 signaling pathway and arsenic-induced apoptosis: a meta-analysis.
Synthesis in Environmental geochemistry and health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Arsenic Exposure Induces Hepatic Fibrosis and Triggers Early Inflammatory Responses by Inhibiting Hepatic Stellate Cell PINK1/Parkin-Mediated Mitophagy.Biological trace element research · 2026Article
- Bak interacts with AKT and is involved in TNFα/CHX-induced apoptosis.Molecular and cellular biochemistry · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic exposure could induce apoptosis and cause related cancer. It was reported that p38 signaling pathway played a key transcriptional regulatory factor in arsenic-induced apoptosis. However, there were certain disputable questions about this point of opinion. Therefore, the relationship between p38 signaling pathway and arsenic-induced apoptosis was systematically reviewed and analyzed by meta-analysis. Twelve essays were analyzed with StataSE15.0 and Review Manager 5.3. The regulatory variables, such as normal cells and cancer cells, arsenic exposure time and exposure dose were analyzed by the subgroup analysis. The comprehensive effects were compared and analyzed by SMD method. Publication bias, the monolithic impact and heterogeneity were inspected. Subgroup analysis showed, when arsenic exposure was ≥ 5 μmol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated. When arsenic exposure was < 5 μmol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated. Arsenic exposure time (≥ 48 h) or arsenic exposure dose (≥ 5 μmol/l or < 5 μmol/l) can promote the expression of p38. Arsenic exposure time was ≥ 48 h or exposure dose was < 5 μmol/l in cancer cells, arsenic exposure dose was ≥ 5 μmol/l or exposure time was < 48 h in normal cells, and they are statistically significant in the expression of p38. This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.
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