Evidence map›Paper›PMID 33393204›Full record

ReviewThe FEBS journal2021

Metabolic requirements of pulmonary fibrosis: role of fibroblast metabolism.

Robert B Hamanaka, Gökhan M Mutlu

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Trained immunity in respiratory diseases: Mechanisms of action and intervention strategies.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025
    Review
  10. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Self-assembled vectors derived fromMaterials today. Bio · 2025
    Article
  16. Article
  17. Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025
    Article
  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

2 authors at 1 institution in 1 country.

Robert B HamanakaSection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, IL, USA.ORCID 0000-0002-8909-356X
Gökhan M MutluSection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, IL, USA.ORCID 0000-0002-2056-612X
University of Chicago · US

Funding

Pilot Program CoreP30ES027792 · NIEHS · UNIVERSITY OF CHICAGO · PI Gokhan M. Mutlu, Gail S Prins · 2017 to 2026
$13.6M
Mechanisms Underlying Sympathetic Activation-dependent Endothelial Cell Activation by Chronic Intermittent HypoxiaP01HL144454 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2019 to 2023
$12.7M
Role of alveolar macrophages in particulate matter-induced cardiopulmonary diseaseR01ES015024 · NIEHS · UNIVERSITY OF CHICAGO · PI MUTLU, GOKHAN M. · 2006 to 2022
$6.1M
Particulate matter-induced changes in DNA methylome and transcriptomeU01ES026718 · NIEHS · UNIVERSITY OF CHICAGO · PI MUTLU, GOKHAN M. · 2016 to 2019
$2.5M
Metabolic Regulation of Myofibroblast DifferentiationR01HL151680 · NHLBI · UNIVERSITY OF CHICAGO · PI HAMANAKA, ROBERT BRIAN · 2020 to 2024
$2.0M
NHLBI NIH HHS P01 HL144454NHLBI NIH HHS R01 HL151680NIEHS NIH HHS P30 ES027792NIEHS NIH HHS R01 ES015024NIEHS NIH HHS U01 ES026718
6 · The paper itself

Abstract

Fibrosis is a pathologic condition characterized by excessive deposition of extracellular matrix and chronic scaring that can affect every organ system. Organ fibrosis is associated with significant morbidity and mortality, contributing to as many as 45% of all deaths in the developed world. In the lung, many chronic lung diseases may lead to fibrosis, the most devastating being idiopathic pulmonary fibrosis (IPF), which affects approximately 3 million people worldwide and has a median survival of 3.8 years. Currently approved therapies for IPF do not significantly extend lifespan, and thus, there is pressing need for novel therapeutic strategies to treat IPF and other fibrotic diseases. At the heart of pulmonary fibrosis are myofibroblasts, contractile cells with characteristics of both fibroblasts and smooth muscle cells, which are the primary cell type responsible for matrix deposition in fibrotic diseases. Much work has centered around targeting the extracellular growth factors and intracellular signaling regulators of myofibroblast differentiation. Recently, metabolic changes associated with myofibroblast differentiation have come to the fore as targetable mechanisms required for myofibroblast function. In this review, we will discuss the metabolic changes associated with myofibroblast differentiation, as well as the mechanisms by which these changes promote myofibroblast function. We will then discuss the potential for this new knowledge to lead to the development of novel therapies for IPF and other fibrotic diseases.

Indexed as

AnimalsFibroblastsFibrosisHumansbioenergeticsfibroblastmetabolismmitochondriapulmonary fibrosis

Identifiers

PMID33393204
PMCPMC8253875
OpenAlexW3119881275

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.