Evidence map›Paper›PMID 35165165›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

TFAM-Dependent Mitochondrial Metabolism Is Required for Alveolar Macrophage Maintenance and Homeostasis.

Xiaochen Gao, Bibo Zhu, Yue Wu, Chaofan Li, Xian Zhou, Jinyi Tang, Jie Sun

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
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  8. Article
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  12. RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. The deadly dance of alveolar macrophages and influenza virus.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  18. Article
  19. Review
  20. 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

7 authors at 3 institutions in 1 country.

Xiaochen GaoDepartment of Immunology, Mayo Clinic, Rochester, MN.
Bibo ZhuDepartment of Immunology, Mayo Clinic, Rochester, MN.
Yue WuDepartment of Immunology, Mayo Clinic, Rochester, MN.ORCID 0000-0003-3667-2960
Chaofan LiDepartment of Immunology, Mayo Clinic, Rochester, MN.ORCID 0000-0002-5426-1498
Xian ZhouDepartment of Immunology, Mayo Clinic, Rochester, MN.
Jinyi TangDepartment of Immunology, Mayo Clinic, Rochester, MN.
Jie SunDepartment of Immunology, Mayo Clinic, Rochester, MN; js6re@virginia.edu.ORCID 0000-0002-2347-4511
Mayo Clinic in Arizona · USCarter Center · USMayo Clinic · US

Funding

Host cellular network governing the development of post SARS-CoV-2 tissue sequelaeR01AI147394 · NIAID · UNIVERSITY OF VIRGINIA · PI Jie Sun · 2020 to 2026
$4.7M
Molecular regulation of protective CD8 immunity against influenza infectionR01AI112844 · NIAID · UNIVERSITY OF VIRGINIA · PI SUN, JIE · 2015 to 2024
$4.5M
Elucidating the roles of alveolar macrophage inflammation and selfrenewal during influenza infectionR01AG069264 · NIA · UNIVERSITY OF VIRGINIA · PI Jie Sun · 2020 to 2026
$3.5M
Roles of tissue-resident helper T cells in mucosal immunity against influenzainfectionR01AI154598 · NIAID · UNIVERSITY OF VIRGINIA · PI SUN, JIE · 2020 to 2024
$2.9M
Simultaneously boosting both humoral and cellular immunity following vaccinationR01AG047156 · NIA · MAYO CLINIC ROCHESTER · PI SUN, JIE · 2015 to 2019
$1.6M
NIAID NIH HHS R01 AI112844NIAID NIH HHS R01 AI147394NIAID NIH HHS R01 AI154598NIA NIH HHS R01 AG047156NIA NIH HHS R01 AG069264
6 · The paper itself

Abstract

Alveolar macrophages (AMs) are major lung tissue-resident macrophages capable of proliferating and self-renewal in situ. AMs are vital in pulmonary antimicrobial immunity and surfactant clearance. The mechanisms regulating AM compartment formation and maintenance remain to be fully elucidated currently. In this study, we have explored the roles of mitochondrial transcription factor A (TFAM)-mediated mitochondrial fitness and metabolism in regulating AM formation and function. We found that TFAM deficiency in mice resulted in significantly reduced AM numbers and impaired AM maturation in vivo. TFAM deficiency was not required for the generation of AM precursors nor the differentiation of AM precursors into AMs, but was critical for the maintenance of AM compartment. Mechanistically, TFAM deficiency diminished gene programs associated with AM proliferation and self-renewal and promoted the expression of inflammatory genes in AMs. We further showed that TFAM-mediated AM compartment impairment resulted in defective clearance of cellular debris and surfactant in the lung and increased the host susceptibility to severe influenza virus infection. Finally, we found that influenza virus infection in AMs led to impaired TFAM expression and diminished mitochondrial fitness and metabolism. Thus, our data have established the critical function of TFAM-mediated mitochondrial metabolism in AM maintenance and function.

Indexed as

Influenza, HumanOrthomyxoviridae InfectionsAnimalsDNA-Binding ProteinsHigh Mobility Group ProteinsHomeostasisHumansLungMacrophages, AlveolarMiceMice, KnockoutSurface-Active AgentsDNA-Binding ProteinsHigh Mobility Group ProteinsSurface-Active AgentsTfam protein, mouse

Identifiers

PMID35165165
PMCPMC9801487
OpenAlexW4213317799

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.