Evidence map›Paper›PMID 38038714›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2024

Fibroblasts and immune cells: at the crossroad of organ inflammation and fibrosis.

Sasha Smolgovsky, Brandon Theall, Noah Wagner, Pilar Alcaide

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
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  9. Review
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  11. Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Observational
  13. Review
  14. Article
  15. Not Just Neurons: Pain Is Orchestrated in Partnership with Many Non-neuronal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Profibrotic MAIT17 Cells in Peritoneal Fibrosis: A New Kid on the Block?Journal of the American Society of Nephrology : JASN · 2025
    Article
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

4 authors at 1 institution in 1 country.

Sasha SmolgovskyDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts, United States.
Brandon TheallDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts, United States.
Noah WagnerDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts, United States.
Pilar AlcaideDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts, United States.ORCID 0000-0003-3013-3982
Tufts University · US

Funding

Mechanisms of T cell activation in cardiac fibrosis and non-ischemic heart failureR01HL144477 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ALCAIDE ALONSO, MARIA PILAR · 2019 to 2023
$3.2M
Regulation of T cell immune response in Heart Failure with Preserved Ejection FractionR01HL165725 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Maria Pilar Alcaide Alonso · 2023 to 2026
$2.5M
Characterizing mechanisms of T cell-mediated cardiac pathology in Heart Failure with Preserved Ejection FractionF31HL159907 · NHLBI · TUFTS UNIVERSITY BOSTON · PI SMOLGOVSKY, SANDRA · 2022 to 2023
$67k
NHLBI NIH HHS F31 HL159907NHLBI NIH HHS R01 HL144477NHLBI NIH HHS R01 HL165725
6 · The paper itself

Abstract

The immune and fibrotic responses have evolved to work in tandem to respond to pathogen clearance and promote tissue repair. However, excessive immune and fibrotic responses lead to chronic inflammation and fibrosis, respectively, both of which are key pathological drivers of organ pathophysiology. Fibroblasts and immune cells are central to these responses, and evidence of these two cell types communicating through soluble mediators or adopting functions from each other through direct contact is constantly emerging. Here, we review complex junctions of fibroblast-immune cell cross talk, such as immune cell modulation of fibroblast physiology and fibroblast acquisition of immune cell-like functions, as well as how these systems of communication contribute to organ pathophysiology. We review the concept of antigen presentation by fibroblasts among different organs with different regenerative capacities, and then focus on the inflammation-fibrosis axis in the heart in the complex syndrome of heart failure. We discuss the need to develop anti-inflammatory and antifibrotic therapies, so far unsuccessful to date, that target novel mechanisms that sit at the crossroads of the fibrotic and immune responses.

Indexed as

FibroblastsInflammationAnti-Inflammatory AgentsFibrosisHumansAnti-Inflammatory Agentscardiovascularfibroblastsfibrosisimmune cellsinflammation

Identifiers

PMID38038714
PMCPMC11219060
OpenAlexW4389244540

What OpenQuestion holds

Textmetadata
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.