Evidence map›Paper›PMID 33262766›Full record

ReviewFrontiers in immunology2020

Granzyme B in Inflammatory Diseases: Apoptosis, Inflammation, Extracellular Matrix Remodeling, Epithelial-to-Mesenchymal Transition and Fibrosis.

Francesca Velotti, Ilaria Barchetta, Flavia Agata Cimini, Maria Gisella Cavallo

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
  2. Article
  3. Cells · 2026
    Article
  4. Article
  5. Article
  6. Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. CD160Cellular & molecular immunology · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. bioRxiv : the preprint server for biology · 2025
    Article
  15. IL-21-dependent Ly6CCell death discovery · 2025
    Article
  16. Single-Cell RNA Sequencing Reveals Granzyme KJournal of the American Heart Association · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. Article

14 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Francesca VelottiDepartment of Ecological and Biological Sciences (DEB), Tuscia University, Viterbo, Italy.
Ilaria BarchettaDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Flavia Agata CiminiDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Maria Gisella CavalloDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Sapienza University of Rome · ITUniversità degli Studi della Tuscia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is strictly interconnected to anti-inflammatory mechanisms to maintain tissue homeostasis. The disruption of immune homeostasis can lead to acute and chronic inflammatory diseases, as cardiovascular, pulmonary, metabolic diseases and cancer. The knowledge of the mechanisms involved in the development and progression of these pathological conditions is important to find effective therapies. Granzyme B (GrB) is a serine protease produced by a variety of immune, non-immune and tumor cells. Apoptotic intracellular and multiple extracellular functions of GrB have been recently identified. Its capability of cleaving extracellular matrix (ECM) components, cytokines, cell receptors and clotting proteins, revealed GrB as a potential multifunctional pro-inflammatory molecule with the capability of contributing to the pathogenesis of different inflammatory conditions, including inflammaging, acute and chronic inflammatory diseases and cancer. Here we give an overview of recent data concerning GrB activity on multiple targets, potentially allowing this enzyme to regulate a wide range of crucial biological processes that play a role in the development, progression and/or severity of inflammatory diseases. We focus our attention on the promotion by GrB of perforin-dependent and perforin-independent (anoikis) apoptosis, inflammation derived by the activation of some cytokines belonging to the IL-1 cytokine family, ECM remodeling, epithelial-to-mesenchymal transition (EMT) and fibrosis. A greater comprehension of the pathophysiological consequences of GrB-mediated multiple activities may favor the design of new therapies aim to inhibit different inflammatory pathological conditions such as inflammaging and age-related diseases, EMT and organ fibrosis.

Indexed as

AnimalsApoptosisEpithelial-Mesenchymal TransitionExtracellular MatrixFibrosisGranzymesHumansInflammationPerforinGranzymesGZMB protein, humanPerforinanoikisapoptosisepithelial-to-mesenchymal transitionextracellular matrix remodelingfibrosisgranzyme Binflammaginginflammatory cytokines

Identifiers

PMID33262766
PMCPMC7686573
OpenAlexW3098043085

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.