Evidence map›Paper›PMID 31555131›Full record

ArticleFrontiers in pharmacology2019

Cigarette Smoke Reduces Fatty Acid Catabolism, Leading to Apoptosis in Lung Endothelial Cells: Implication for Pathogenesis of COPD.

Jiannan Gong, Hui Zhao, Tanzhen Liu, Lifang Li, Erjing Cheng, Shuyin Zhi, Lufei Kong, Hong-Wei Yao, Jianqiang Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  13. L-carnitine reduces acute lung injury via mitochondria modulation and inflammation control in pulmonary macrophages.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
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  19. Metformin alleviates chronic obstructive pulmonary disease and cigarette smoke extract-induced glucocorticoid resistance by activating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
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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

9 authors at 2 institutions in 1 country.

Jiannan GongDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Hui ZhaoDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Tanzhen LiuDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Lifang LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Erjing ChengDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Shuyin ZhiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Lufei KongDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Hong-Wei YaoDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Jianqiang LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Shanxi Medical University · CNSecond Hospital of Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cell (EC) apoptosis contributes to cigarette smoke (CS)-induced pulmonary emphysema. Metabolism of glucose, glutamine, and fatty acid is dysregulated in patients with chronic obstructive pulmonary disease (COPD). Whether CS causes metabolic dysregulation in ECs leading to development of COPD remains elusive. We hypothesized that CS alters metabolism, resulting in apoptosis in lung ECs. To test this hypothesis, we treated primary mouse pulmonary microvascular ECs (PMVECs) with CS extract (CSE) and employed PMVECs from healthy subjects and COPD patients. We found that mitochondrial respiration was reduced in CSE-treated PMVECs and in PMVECs from COPD patients. Specifically, oxidation of fatty acids (FAO) was reduced in these cells, which linked to reduced carnitine palmitoyltransferase 1a (Cpt1a), an essential enzyme for carnitine shuttle. CSE-induced apoptosis was further increased when cells were treated with a specific Cpt1 inhibitor etomoxir or transfected with Cpt1a siRNA. L-Carnitine treatment augmented FAO but attenuated CSE-induced apoptosis by upregulating Cpt1a. CSE treatment increased palmitate-derived ceramide synthesis, which was reduced by L-carnitine. Although CSE treatment increased glycolysis, inhibiting glycolysis with 2-deoxy-d-glucose had no effects on CSE-mediated apoptosis in lung ECs. Conclusively, FAO reduction increases ceramide and apoptosis in lung ECs treated with CSE, which may contribute to the pathogenesis of COPD/emphysema.

Indexed as

apoptosisceramidechronic obstructive pulmonary diseaseendothelial cellsmetabolism

Identifiers

PMID31555131
PMCPMC6727183
OpenAlexW2963491244

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.