Evidence map›Paper›PMID 41519740›Full record

ArticleBMC pulmonary medicine2026

Biological aging, a mediator between smoking and chronic obstructive pulmonary disease: evidence from a hospital-based cohort study in China.

Dongming Xie, Ao Lin, Feng Luo, Katie Lu, Zhi Li, Jinyi Huang, Jinrong Zhang, Jianjun Zou, Houli Xiao, Zhiyong Ren and 5 more

Abstract read
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In one paragraph

Article in BMC pulmonary medicine, 2026. 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

15 authors.

Dongming XieThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Ao LinDepartment of Thoracic Surgery, The First Affiliated Hospital; School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Feng LuoThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Katie LuSchool of Medicine, University of Arizona, 602 N Highland Ave, Tucson, AZ, 85719, USA.
Zhi LiThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jinyi HuangThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jinrong ZhangThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jianjun ZouDepartment of General Internal Medicine, Guangzhou Chest Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Houli XiaoThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Zhiyong RenThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Dongsheng HuangDepartment of Respiratory and Critical Care Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, Guangdong, China.
Chenli XieDepartment of Respiratory and Critical Care Medicine, Binhaiwan Central Hospital of Dongguan, Dongguan, Guangdong, China.
Cuiyi ChenDepartment of Respiratory and Critical Care Medicine, Songshan Lake Central Hospital of Dongguan, Dongguan, Guangdong, China.
Yibin DengCentre for Medical Laboratory Science; Key Laboratory of Research On Clinical Molecular Diagnosis for High Incidence Diseases in Western Guangxi, the Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China. dengyb75@163.com.
Jiachun LuThe Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China. jclu@gzhmu.edu.cn.

Funding

Dongguan Science and Technology of Social Developmen Programt 20221800905212National Natural Science Foundation of China 82373678National Natural Science Foundation of China,China 82173609Natural Science Foundation of Guangdong Province 2023A1515011627
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity, with aging and smoking as key risk factors. However, the mediating role of biological aging in the smoking-COPD relationship has been rarely examined in Chinese populations.

methodsIn this hospital-based cohort study, 1,269 Chinese adults aged 40-84 years without COPD were enrolled. We developed Klemera-Doubal method-biological age (KDM-BA) using 11 routine clinical biomarkers. KDM-BA acceleration (KDM-BAAc) was calculated by regressing KDM-BA on chronological age (CA). Three Cox models were used to assess the association between KDM-BAAc and COPD risk. Restricted cubic spline models were used to evaluate the dose-response relationship between KDM-BAAc and COPD risk. Counterfactual mediation analysis was used to quantify BA acceleration's mediating role in smoking-COPD association.

resultsOver a mean follow-up of 3.4 years, 47 incident COPD cases occurred (incidence rate: 10.90/1000 person-years). Biological older was associated with higher COPD incidence [15.94 vs. 7.00/1,000 person-years; rate ratios (RR) = 2.28, 95% confidence intervals (95% CI) = 1.22-4.40]. Each 1-year increase in KDM-BAAc elevated COPD risk by 7% [fully adjusted hazard ratio (HR) = 1.07, 95% CI = 1.03-1.12]. Dose-response relationships were found between biological aging and COPD (fully adjusted P

conclusionAccelerated biological aging is associated with increased COPD risk and serves as a significant mediator in the smoking-COPD relationship among Chinese adults.

Indexed as

AgingPulmonary Disease, Chronic ObstructiveSmokingAdultAgedAged, 80 and overBiomarkersChinaCohort StudiesFemaleHumansIncidenceMaleMiddle AgedProportional Hazards ModelsRisk FactorsBiomarkersBiological agingChronic Obstructive Pulmonary DiseaseCohort studyMediation analysisSmoking

Identifiers

PMID41519740
PMCPMC12918538

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.