Molecular Mechanisms of Indoor Environmental Pollution tt-DDE-Induced Blood Pressure Elevation and the Protective Role of Human-Specific Gene CHRFAM7A.

Siwen Li, Ying Su, Peng Fang, Shuzi Ye, Yu Yuan, Lemei Liu, Junchang Wang, Fang Xiao

Abstract read

In one paragraph

Article in Environment & health (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Siwen LiDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.ORCID https://orcid.org/0000-0003-0784-134X

Ying SuDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Peng FangDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Shuzi YeDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Yu YuanDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Lemei LiuDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Junchang WangDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.

Fang XiaoDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan 410013, China.ORCID https://orcid.org/0000-0002-6814-1227

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cooking oil fumes (COFs), a major source of indoor air pollutants, are responsible for approximately 90% of indoor particulate matter emissions. Trans,trans-2,4-decadienal (tt-DDE), the predominant aldehyde in COFs, exhibits established mutagenic and carcinogenic potential. Although CHRFAM7A remains to be validated as a cardiovascular therapeutic target, accumulating evidence positions it as a novel modulator of the cardiovascular pathophysiology. This study explored the protective mechanisms of CHRFAM7A against the tt-DDE-induced vascular injury. First, inhalation of tt-DDE was observed to elevate blood pressure, an effect attributed to associated endothelial cell damage. Additionally, we found that CHRFAM7A-transgenic mice exhibit significant resistance to tt-DDE-induced systolic hypertension and endothelial dysfunction. Mechanistically, the observed protection was attributed to the STAT3/HO-1 pathway activation. Moreover,

Indexed as

Blood pressure elevationCHRFAM7AKrüppel-like factor 5N6-MethyladenosineTrans, trans-2,4-decadienal

Identifiers

PMID42775181

DOI10.1021/envhealth.5c00703

PMCPMC13595388

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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.