Evidence map›Paper›PMID 40469988›Full record

ReviewFrontiers in pharmacology2025

Modulating mitochondria with natural extract compounds: from bench to clinical therapeutic opportunities for COPD.

Qiao Wang, Ziling Zeng, Linlin Guo, Kent E Williams, Yun Zhang, Hongmei Tang, Hang Hu, Gang Qin, Kaijin Wang, Xing Wang

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Qiao Wang *Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Ziling Zeng *Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Linlin Guo *Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, United States.
Kent E WilliamsIndiana University School of Medicine, Melvin and Bren Simon Comprehensive Cancer Center, Indianapolis, IN, United States.
Yun ZhangInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Hongmei TangInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Hang HuDepartment of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Gang QinDepartment of Otolaryngology Head and Neck Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Kaijin WangDepartment of Respiratory and Critical Care Medicine, Bishan Hospital of Chongqing, Bishan Hospital of Chongqing Medical University, Chongqing, China.
Xing WangInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease that leads to death and disability worldwide, and it is caused by hereditary and environmental factors. It is characterized by chronic inflammation, emphysema, and irreversible limitation of airflow. Dual or triple therapy with a traditional approach can provide relief from COPD symptoms by reducing the frequency and severity of the outbreaks, but there are no current therapies to reverse the long-term decline in lung function. Although ICS rescue inhalers demonstrate efficacy in acute attacks, these cannot be utilized for chronic management of COPD due to adverse effects. Therefore, novel agents and therapeutic strategies are urgently needed to address this disease. It is believed that malfunctioning mitochondria are associated with COPD pathogenesis, contributing to inflammation, apoptosis, and cellular senescence. A better understanding of these mechanisms could provide novel therapeutic approaches for maintaining lung and skeletal muscle function. Many natural extract compounds show therapeutic potential for COPD and are associated with few adverse reactions. Notably, these natural compounds can improve mitochondrial function and exhibit a variety of anti-inflammatory, antioxidant, and immunomodulatory properties. In this review, we systemically summarize the pathogenic role of impaired mitochondria in COPD and the potential mechanisms by which natural extract compounds may ameliorate these impairments.

Indexed as

cigarette smokeCOPDlung diseaseMitochondriamtROSnatural extract compound

Identifiers

PMID40469988
PMCPMC12133498

What OpenQuestion holds

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Registered trials

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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.