Evidence map›Paper›PMID 32722485›Full record

ReviewInternational journal of molecular sciences2020

HSP90 Inhibition and Modulation of the Proteome: Therapeutical Implications for Idiopathic Pulmonary Fibrosis (IPF).

Ruben Manuel Luciano Colunga Biancatelli, Pavel Solopov, Betsy Gregory, John D Catravas

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Herbacetin as a novel therapeutic agent for pulmonary and renal fibrosis by targeting TGFBR2 for degradation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. The role of heat shock protein 90 in idiopathic pulmonary fibrosis: state of the art.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Ceapin-A7 potentiates lipopolysaccharide-induced endothelial injury.Journal of biochemical and molecular toxicology · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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 2 institutions in 2 countries.

Ruben Manuel Luciano Colunga BiancatelliFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Pavel SolopovFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.ORCID 0000-0002-1705-027X
Betsy GregoryFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
John D CatravasFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Old Dominion University · USPoliclinico Umberto I · IT

Funding

Antidotes against HCI-induced chronic lung injuryU01ES030674 · NIEHS · OLD DOMINION UNIVERSITY · PI CATRAVAS, JOHN D · 2020 to 2022
$1.4M
Antidotes against mustard-induced chronic lung injuryR21ES030528 · NIEHS · OLD DOMINION UNIVERSITY · PI CATRAVAS, JOHN D · 2018 to 2019
$426k
NIEHS NIH HHS R21 ES030528NIEHS NIH HHS U01 ES030674NIH Office of the Director R21ES029309, R21ES030528, U01ES030674
6 · The paper itself

Abstract

Idiopathic Pulmonary fibrosis (IPF) is a catastrophic disease with poor outcomes and limited pharmacological approaches. Heat shock protein 90 (HSP90) has been recently involved in the wound-healing pathological response that leads to collagen deposition in patients with IPF and its inhibition represents an exciting drug target against the development of pulmonary fibrosis. Under physiological conditions, HSP90 guarantees proteostasis through the refolding of damaged proteins and the degradation of irreversibly damaged ones. Additionally, its inhibition, by specific HSP90 inhibitors (e.g., 17 AAG, 17 DAG, and AUY-922) has proven beneficial in different preclinical models of human disease. HSP90 inhibition modulates a complex subset of kinases and interferes with intracellular signaling pathways and proteome regulation. In this review, we evaluated the current evidence and rationale for the use of HSP90 inhibitors in the treatment of pulmonary fibrosis, discussed the intracellular pathways involved, described the limitations of the current understanding and provided insights for future research.

Indexed as

Idiopathic Pulmonary FibrosisProteostasisSignal TransductionAnimalsHSP90 Heat-Shock ProteinsHumansProteomeHSP90 Heat-Shock ProteinsProteome17 AAGAUY-922ERKHSP90HSP90 inhibitorHSPomeIdiopathic Pulmonary FibrosisProteomeProteomicsTGF-β

Identifiers

PMID32722485
PMCPMC7432830
OpenAlexW3045085464

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.