ArticleEnvironmental science and pollution research international2018
In type 2 diabetes induced by cigarette smoking, activation of p38 MAPK is involved in pancreatic β-cell apoptosis.
Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Oxidative stress and type 2 diabetes: a review of lactic acid bacteria as potential prophylactic and therapeutic interventions.Food science and biotechnology · 2025Review
- Type 2 Diabetes Mellitus in Tanzania. A Narrative Review of Epidemiology and Disease Trend.Current diabetes reviews · 2024Review
- miR-153-3p via PIK3R1 Is Involved in Cigarette Smoke-Induced Neurotoxicity in the Brain.Toxics · 2023Article
- Xenobiotics Delivered by Electronic Nicotine Delivery Systems: Potential Cellular and Molecular Mechanisms on the Pathogenesis of Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis.Molecules (Basel, Switzerland) · 2022Article
- Causal effect of education on type 2 diabetes: A network Mendelian randomization study.World journal of diabetes · 2021Article
- Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet.International journal of molecular sciences · 2020Article
- Observational
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Type 2 diabetes (T2D) is a chronic disease caused by pancreatic β-cell dysfunction and insulin resistance. Exposure to smoke is a risk factor for diabetes; however, its mechanisms are unclear. In an epidemiological study, we determined the relationship between cigarette smoking and β-cell function. T2D patients had a history of heavier smoking than people without T2D, and heavy smokers had more abnormal glucose metabolism. For various smoking populations, there was a dose-effect relationship between decreases of homeostatic model assessment (HOMA)-β levels or the increases of HOMA-insulin resistance (IR) levels and amount of smoking (pack-years), which indicated that smoking induced β-cell dysfunction. For MIN6 cells, cigarette smoke extract (CSE) decreased insulin secretion and content; enhanced apoptosis, as illustrated by decreases of BCL-2 levels, increases of BAX and cleaved caspase-3 levels, and an increased apoptotic index; and activated the p38 MAPK pathway. For MIN6 cells, inhibition of p-p38 MAPK by SB203580 prevented enhanced apoptosis and the dysfunction of insulin secretion induced by CSE. In sum, activation of p38 MAPK is involved in the apoptosis of pancreatic β-cells induced by cigarette smoking, which is a possible mechanism for induction of T2D by cigarette smoke.
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