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Background <p>Emphysema is a predominant pathological feature of chronic obstructive pulmonary disease (COPD) and is closely associated with cigarette smoke (CS) exposure. Cigarette smoke extract (CSE) provides a controlled in vitro platform for elucidating the molecular mechanisms underlying smoke-induced injury, whereas whole CS models more faithfully reproduce the chronic exposure dynamics and systemic effects characteristic of human smoking.</p> Materials and methods <p>A systematic search of PubMed and Scopus (2000–2025) identified 6,192 records. Following screening via the PECO framework and a PRISMA-based approach, 66 studies investigating CS- or CSE-induced emphysema met the inclusion criteria. Bibliometric analyses were conducted via the Bibliometrix R package.</p> Results <p>CS-induced emphysema research has focused predominantly on North America and Asia and emphasizes systemic pathology and clinically relevant disease features. In contrast, CSE-based studies, largely concentrated in Asia, focus primarily on cellular and molecular mechanisms, particularly oxidative stress, apoptosis, and epigenetic regulation. Bibliometric mapping revealed significant associations among publication output, citation patterns, collaborative networks, and keyword evolution, highlighting distinct model-dependent research trajectories.</p> Conclusion <p>The CS and CSE models provide complementary yet distinct perspectives on emphysema pathogenesis. While CS models capture chronic structural and systemic disease features, CSE models enable detailed investigations of cellular and molecular mechanisms. Importantly, this bibliometric analysis identifies a model-driven divergence in mechanistic focus and translational orientation that is not apparent from prior narrative reviews, underscoring the need to integrate evidence from both approaches to increase translational relevance in COPD research.</p>

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Two decades of experimental insights into cigarette smoke- and extract-induced emphysema: a bibliographic review (2000–2025)

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月16日

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  • Sneha Sekar,
  • Shanthi Mathialagan,
  • Divya Vinayachandran,
  • Ganesh Chakkarai,
  • Srishta Radhakrishnan,
  • Vigneshwaran K

摘要

Background

Emphysema is a predominant pathological feature of chronic obstructive pulmonary disease (COPD) and is closely associated with cigarette smoke (CS) exposure. Cigarette smoke extract (CSE) provides a controlled in vitro platform for elucidating the molecular mechanisms underlying smoke-induced injury, whereas whole CS models more faithfully reproduce the chronic exposure dynamics and systemic effects characteristic of human smoking.

Materials and methods

A systematic search of PubMed and Scopus (2000–2025) identified 6,192 records. Following screening via the PECO framework and a PRISMA-based approach, 66 studies investigating CS- or CSE-induced emphysema met the inclusion criteria. Bibliometric analyses were conducted via the Bibliometrix R package.

Results

CS-induced emphysema research has focused predominantly on North America and Asia and emphasizes systemic pathology and clinically relevant disease features. In contrast, CSE-based studies, largely concentrated in Asia, focus primarily on cellular and molecular mechanisms, particularly oxidative stress, apoptosis, and epigenetic regulation. Bibliometric mapping revealed significant associations among publication output, citation patterns, collaborative networks, and keyword evolution, highlighting distinct model-dependent research trajectories.

Conclusion

The CS and CSE models provide complementary yet distinct perspectives on emphysema pathogenesis. While CS models capture chronic structural and systemic disease features, CSE models enable detailed investigations of cellular and molecular mechanisms. Importantly, this bibliometric analysis identifies a model-driven divergence in mechanistic focus and translational orientation that is not apparent from prior narrative reviews, underscoring the need to integrate evidence from both approaches to increase translational relevance in COPD research.