Evidence map›Paper›PMID 33387604›Full record

ReviewFree radical biology & medicine2021

Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases.

Linhui Li, David C Yang, Ching-Hsien Chen

Open access · bronzeAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 12% of its field
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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. CYP1B1 Mediates Cigarette Smoke-Induced Lipid Accumulation in Alveolar Type 2 Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Oxidative Stress and Lung Fibrosis: Towards an Adverse Outcome Pathway.International journal of molecular sciences · 2023
    Review
  20. Advanced Materials Design for Adsorption of Toxic Substances in Cigarette Smoke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
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

3 authors at 1 institution in 1 country.

Linhui LiDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Center for Comparative Respiratory Biology and Medicine, University of California Davis, Davis, CA, USA; Division of Nephrology, Department of Internal Medicine, University of California Davis, Davis, CA, USA.
David C YangDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Center for Comparative Respiratory Biology and Medicine, University of California Davis, Davis, CA, USA.
Ching-Hsien ChenDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Center for Comparative Respiratory Biology and Medicine, University of California Davis, Davis, CA, USA; Division of Nephrology, Department of Internal Medicine, University of California Davis, Davis, CA, USA. Electronic address: jchchen@ucdavis.edu.
University of California, Davis · US

Funding

TRAINING IN COMPARATIVE LUNG BIOLOGY AND MEDICINET32HL007013 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI Elena Goncharova, Nicholas J. KENYON · 1985 to 2026
$10.1M
Novel role of phospho-MARCKS in macrophages during tobacco smoke-driven fibrosisR01HL146802 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Ching-Hsien Chen · 2019 to 2026
$2.6M
NHLBI NIH HHS R01 HL146802NHLBI NIH HHS T32 HL007013
6 · The paper itself

Abstract

Cigarette smoking is a well-known risk factor for pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary fibrosis. Despite major progress in dissecting the mechanisms associated with disease development and progression, findings only represent one aspect of multifaceted disease. A crucial consequence of this approach is that many therapeutic treatments often fail to improve or reverse the disease state as other conditions and variables are insufficiently considered. To expand our understanding of pulmonary diseases, omics approaches, particularly metabolomics, has been emerging in the field. This strategy has been applied to identify putative biomarkers and novel mechanistic insights. In this review, we discuss metabolic profiles of patients with COPD, asthma, and idiopathic pulmonary fibrosis (IPF) with a focus on the direct effects of cigarette smoking in altering metabolic regulation. We next present cell- and animal-based experiments and point out the therapeutic potential of targeting metabolic reprogramming in inflammatory lung diseases. In addition, the obstacles in translating these findings into clinical practice, including potential adverse effects and limited pharmacological efficacy, are also addressed.

Indexed as

AsthmaCigarette SmokingIdiopathic Pulmonary FibrosisPulmonary Disease, Chronic ObstructiveAnimalsHumansLungSmokeSmokeAsthmaCellular metabolismCOPDIPFSmoking

Identifiers

PMID33387604
PMCPMC7870291
OpenAlexW3113886568

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.