Evidence map›Paper›PMID 27704718›Full record

ArticleJournal of cellular and molecular medicine2017

HYDAMTIQ, a selective PARP-1 inhibitor, improves bleomycin-induced lung fibrosis by dampening the TGF-β/SMAD signalling pathway.

Laura Lucarini, Mariaconcetta Durante, Cecilia Lanzi, Alessandro Pini, Giulia Boccalini, Laura Calosi, Flavio Moroni, Emanuela Masini, Guido Mannaioni

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Antioxidant therapy against TGF-β/SMAD pathway involved in organ fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  8. Role of histamine HInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  9. Review
  10. Review
  11. Adenosine AInternational journal of molecular sciences · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Effects ofFrontiers in pharmacology · 2021
    Article
  18. Poly(ADP-Ribose) Polymerase Inhibition in Acute Lung Injury. A Reemerging Concept.American journal of respiratory cell and molecular biology · 2020
    Review
  19. Article
  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

9 authors at 1 institution in 1 country.

Laura LucariniDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
Mariaconcetta DuranteDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
Cecilia LanziDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
Alessandro PiniDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy.
Giulia BoccaliniDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy.
Laura CalosiDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy.
Flavio MoroniDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
Emanuela MasiniDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
Guido MannaioniDepartment of Neuroscience, Psychiatry, Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis is a severe disease characterized by excessive myofibroblast proliferation, extracellular matrix and fibrils deposition, remodelling of lung parenchyma and pulmonary insufficiency. Drugs able to reduce disease progression are available, but therapeutic results are unsatisfactory; new and safe treatments are urgently needed. Poly(ADP-ribose) polymerases-1 (PARP-1) is an abundant nuclear enzyme involved in key biological processes: DNA repair, gene expression control, and cell survival or death. In liver and heart, PARP-1 activity facilitates oxidative damage, collagen deposition and fibrosis development. In this study, we investigated the effects of HYDAMTIQ, a potent PARP-1 inhibitor, in a murine model of lung fibrosis. We evaluated the role of PARP on transforming growth factor-β (TGF-β) expression and TGF-β/SMAD signalling pathway in lungs. Mice were intratracheally injected with bleomycin and then treated with either vehicle or different doses of HYDAMTIQ for 21 days. Airway resistance to inflation and lung static compliance, markers of lung stiffness, were assayed. Histochemical and biochemical parameters to evaluate TGF-β/SMAD signalling pathway with alpha-smooth muscle actin (αSMA) deposition and the levels of a number of inflammatory markers (tumour necrosis factor-α, interleukin-1β, iNOS and COX-2) were performed. Bleomycin administration increased lung stiffness. It also increased lung PARP activity, TGF-β levels, pSMAD3 expression, αSMA deposition and content of inflammatory markers. HYDAMTIQ attenuated all the above-mentioned physiological, biochemical and histopathological markers. Our findings support the proposal that PARP inhibitors could have a therapeutic potential in reducing the progression of signs and symptoms of the disease by decreasing TGF-β expression and the TGF-β/SMAD transduction pathway.

Indexed as

ActinsAnimalsBiomarkersBleomycinFibroblastsHydroxyprolineInflammation MediatorsIsoquinolinesLungMaleMice, Inbred C57BLOxidative StressPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPulmonary FibrosisSignal Transduction2-((dimethylamino)methyl)-9-hydroxythieno(2,3-c)isoquinolin-5(4H)-oneActa2 protein, mouseActinsBiomarkersBleomycinHydroxyprolineInflammation MediatorsIsoquinolinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesSmad ProteinsThiophenesTransforming Growth Factor betaHYDAMTIQPAOROSSMADαSMA

Identifiers

PMID27704718
PMCPMC5264150
OpenAlexW2527762646

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.