Evidence map›Paper›PMID 29351446›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2018

Mechanisms and consequences of oxidative stress in lung disease: therapeutic implications for an aging populace.

Louise Hecker

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
15.2field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

  1. Pooled it
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  18. Oxidative stress and food as medicine.Frontiers in nutrition · 2024
    Review
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19 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

1 author at 1 institution in 1 country.

Louise HeckerDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona , Tucson, Arizona and Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona.
University of Arizona · US

Funding

Preclinical development of a novel Nrf2-activator formulation for the treatment of idiopathic pulmonary fibrosisR21AG054766 · NIA · UNIVERSITY OF ARIZONA · PI HECKER, LOUISE, MANSOUR, HEIDI M. · 2017 to 2018
$415k
The role of Nampt in age-associated persistent lung fibrosisI01BX003919 · VA · VETERANS HEALTH ADMINISTRATION · PI HECKER, LOUISE · 2018 to 2022
–
Aging, Fibroblast Senescence, and Apoptosis in Lung FibrosisIK2BX001477 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI HECKER, LOUISE · 2012 to 2016
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BLRD VA I01 BX003919BLRD VA IK2 BX001477NIA NIH HHS R21 AG054766
6 · The paper itself

Abstract

The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic and acute lung diseases. Numerous studies have implicated aging and oxidative stress in the pathogenesis of various pulmonary diseases; however, despite recent advances in these fields, the specific contributions of aging and oxidative stress remain elusive. This review will discuss the consequences of aging on lung morphology and physiology, and how redox imbalance with aging contributes to lung disease susceptibility. Here, we focus on three lung diseases for which aging is a significant risk factor: acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Preclinical and clinical development for redox- and senescence-altering therapeutic strategies are discussed, as well as scientific advancements that may direct current and future therapeutic development. A deeper understanding of how aging impacts normal lung function, redox balance, and injury-repair processes will inspire the development of new therapies to prevent and/or reverse age-associated pulmonary diseases, and ultimately increase health span and longevity. This review is intended to encourage basic, clinical, and translational research that will bridge knowledge gaps at the intersection of aging, oxidative stress, and lung disease to fuel the development of more effective therapeutic strategies for lung diseases that disproportionately afflict the elderly.

Indexed as

AgingOxidative StressAnimalsHumansLung Diseaseslung agingoxidative stresssenescence

Identifiers

PMID29351446
PMCPMC5966777
OpenAlexW2780590908

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.