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Objective <p>Cigarette smoking alters lipid metabolism in the lung, but the effects of heated tobacco products (HTPs) remain unclear. We aimed to investigate potential lipidomic alterations in lung and lung cancer tissues associated with HTP exposure.</p> Results <p>We performed lipidomic analysis on specimens from lung adenocarcinoma (LAD) and spontaneous pneumothorax patients. Frozen cancer and adjacent normal lung tissues from LAD cases and lung tissues from pneumothorax cases were analyzed using liquid chromatography–tandem mass spectrometry. Relative intensities of 24 lipid classes were compared among the HTP-user, cigarette-smoker, and never-smoker groups (two cases for each group). In LAD cases, the HTP-user group exhibited high levels of acylcarnitine (AcCa), coenzyme Q10 (CoQ10), triglyceride (TG), and phosphatidylethanolamine in cancer tissue, and CoQ10, TG and monohexosylceramide in normal lung tissue. Cholesteryl ester and cholesterol were consistently low in both cancer and normal lung tissues, while multiple lysophospholipids (lysosphingomyelin, lysophosphatidylethanolamine, lysophosphatidylcholine) and phosphatidylserine were low in normal lung tissue. In pneumothorax cases, CoQ10 was high and AcCa low in HTP-users, though similar patterns were observed in cigarette-smokers. This exploratory pilot study suggests that HTP use may induce oxidative stress–driven metabolic reprogramming, membrane remodeling, and stress-adaptive responses in lung and lung cancer tissues.</p>

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Lipidomic signatures in lung adenocarcinoma and spontaneous pneumothorax tissues associated with heated tobacco use: a pilot study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月28日

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  • Yusuke Takanashi,
  • Takuya Kitamoto,
  • Minako Kondo,
  • Kensuke Takei,
  • Motohisa Shibata,
  • Keigo Sekihara,
  • Kazuhito Funai

摘要

Objective

Cigarette smoking alters lipid metabolism in the lung, but the effects of heated tobacco products (HTPs) remain unclear. We aimed to investigate potential lipidomic alterations in lung and lung cancer tissues associated with HTP exposure.

Results

We performed lipidomic analysis on specimens from lung adenocarcinoma (LAD) and spontaneous pneumothorax patients. Frozen cancer and adjacent normal lung tissues from LAD cases and lung tissues from pneumothorax cases were analyzed using liquid chromatography–tandem mass spectrometry. Relative intensities of 24 lipid classes were compared among the HTP-user, cigarette-smoker, and never-smoker groups (two cases for each group). In LAD cases, the HTP-user group exhibited high levels of acylcarnitine (AcCa), coenzyme Q10 (CoQ10), triglyceride (TG), and phosphatidylethanolamine in cancer tissue, and CoQ10, TG and monohexosylceramide in normal lung tissue. Cholesteryl ester and cholesterol were consistently low in both cancer and normal lung tissues, while multiple lysophospholipids (lysosphingomyelin, lysophosphatidylethanolamine, lysophosphatidylcholine) and phosphatidylserine were low in normal lung tissue. In pneumothorax cases, CoQ10 was high and AcCa low in HTP-users, though similar patterns were observed in cigarette-smokers. This exploratory pilot study suggests that HTP use may induce oxidative stress–driven metabolic reprogramming, membrane remodeling, and stress-adaptive responses in lung and lung cancer tissues.