Evidence map›Paper›PMID 34943963›Full record

ReviewCells2021

Senescence Alterations in Pulmonary Hypertension.

Inés Roger, Javier Milara, Nada Belhadj, Julio Cortijo

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Frailty in Pulmonary Hypertension: A Multidimensional Comorbidity.Annals of the American Thoracic Society · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Cell Death in Pulmonary Arterial Hypertension.International journal of medical sciences · 2024
    Review
  18. Review
  19. Article
  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

4 authors at 3 institutions in 1 country.

Inés RogerCentro de Investigación en Red Enfermedades Respiratorias CIBERES, Health Institute Carlos III, 28029 Valencia, Spain.
Javier MilaraCentro de Investigación en Red Enfermedades Respiratorias CIBERES, Health Institute Carlos III, 28029 Valencia, Spain.
Nada BelhadjDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Julio CortijoCentro de Investigación en Red Enfermedades Respiratorias CIBERES, Health Institute Carlos III, 28029 Valencia, Spain.
Universitat de València · ESCentro de Investigación Biomédica en Red de Enfermedades Respiratorias · ESHospital General Universitario De Valencia · ES

Funding

CIBERES CB06 / 06/0027Fondo Europeo de Desarrollo Regional (FEDER) and Instituto de salud carlos III PI20 / 01363Regional Government Prometeo 2017/023 / UVSpanish Government PID2020-114871RB-I00
6 · The paper itself

Abstract

Cellular senescence is the arrest of normal cell division and is commonly associated with aging. The interest in the role of cellular senescence in lung diseases derives from the observation of markers of senescence in chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (IPF), and pulmonary hypertension (PH). Accumulation of senescent cells and the senescence-associated secretory phenotype in the lung of aged patients may lead to mild persistent inflammation, which results in tissue damage. Oxidative stress due to environmental exposures such as cigarette smoke also promotes cellular senescence, together with additional forms of cellular stress such as mitochondrial dysfunction and endoplasmic reticulum stress. Growing recent evidence indicate that senescent cell phenotypes are observed in pulmonary artery smooth muscle cells and endothelial cells of patients with PH, contributing to pulmonary artery remodeling and PH development. In this review, we analyze the role of different senescence cell phenotypes contributing to the pulmonary artery remodeling process in different PH clinical entities. Different molecular pathway activation and cellular functions derived from senescence activation will be analyzed and discussed as promising targets to develop future senotherapies as promising treatments to attenuate pulmonary artery remodeling in PH.

Indexed as

AgingCellular SenescenceEndothelial CellsHumansHypertension, PulmonaryInflammationLungOxidative StressPulmonary ArteryPulmonary Disease, Chronic ObstructivePulmonary Fibrosispulmonary hypertensionSASPsenescencesenolytics

Identifiers

PMID34943963
PMCPMC8700581
OpenAlexW4200189209

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.