Evidence map›Paper›PMID 32037306›Full record

ReviewRedox biology2020

Cellular stress responses and dysfunctional Mitochondrial-cellular senescence, and therapeutics in chronic respiratory diseases.

Marko Manevski, Thivanka Muthumalage, Dinesh Devadoss, Isaac K Sundar, Qixin Wang, Kameshwar P Singh, Hoshang J Unwalla, Hitendra S Chand, Irfan Rahman

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
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  4. β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026
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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 2 institutions in 1 country.

Marko ManevskiDepartment of Immunology and NanoMedicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Thivanka MuthumalageDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Dinesh DevadossDepartment of Immunology and NanoMedicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Isaac K SundarDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Qixin WangDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Kameshwar P SinghDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Hoshang J UnwallaDepartment of Immunology and NanoMedicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Hitendra S ChandDepartment of Immunology and NanoMedicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Irfan RahmanDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA. Electronic address: irfan_rahman@urmc.rochester.edu.
University of Rochester Medical Center · USFlorida International University · US

Funding

HIV-associated Chronic Obstructive Pulmonary DiseaseR01HL125000 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI MISHRA, NEERAD, SOPORI, MOHAN L. · 2014 to 2017
$3.0M
Inflammatory and Dysregulated Repair Responses to Inhaled NicotineR01HL135613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2017 to 2021
$2.7M
Mechanisms of Defective Mitophagy and cellular Senescence in HIV-associated COPDR01HL147715 · NHLBI · FLORIDA INTERNATIONAL UNIVERSITY · PI IRFAN RAHMAN, HOSHANG JEHANGIR UNWALLA · 2019 to 2026
$2.6M
Nuclear Receptor REV-ERB alpha Role in the Pathophysiology of Allergic AsthmaR01HL142543 · NHLBI · UNIVERSITY OF ROCHESTER · PI SUNDAR, ISAAC KIRUBAKARAN · 2019 to 2023
$1.9M
Mechanism of Mitochondrial Dysfunction in COPDR01HL137738 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2017 to 2020
$1.5M
Molecular Clock REV-ERBα in COPD and its exacerbationsR01HL133404 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2017 to 2020
$1.5M
Novel long noncoding RNAs in the airway mucous responseR21AI144374 · NIAID · FLORIDA INTERNATIONAL UNIVERSITY · PI LAKSHMANA, MADEPALLI KRISHNAPPA · 2019 to 2020
$625k
Targeting Hyperplastic Airway Cells Using a Small Molecule InhibitorR21AI117560 · NIAID · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI CHAND, HITENDRA SINGH · 2016 to 2017
$510k
Exosomes in Environmental Tobacco Smoke-induced Lung Cellular SenescenceR21ES028006 · NIEHS · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2017 to 2018
$423k
NHLBI NIH HHS R01 HL125000NHLBI NIH HHS R01 HL133404NHLBI NIH HHS R01 HL135613NHLBI NIH HHS R01 HL137738NHLBI NIH HHS R01 HL142543NHLBI NIH HHS R01 HL147715NIAID NIH HHS R21 AI117560NIAID NIH HHS R21 AI144374NIEHS NIH HHS R21 ES028006
6 · The paper itself

Abstract

The abnormal inflammatory responses due to the lung tissue damage and ineffective repair/resolution in response to the inhaled toxicants result in the pathological changes associated with chronic respiratory diseases. Investigation of such pathophysiological mechanisms provides the opportunity to develop the molecular phenotype-specific diagnostic assays and could help in designing the personalized medicine-based therapeutic approaches against these prevalent diseases. As the central hubs of cell metabolism and energetics, mitochondria integrate cellular responses and interorganellar signaling pathways to maintain cellular and extracellular redox status and the cellular senescence that dictate the lung tissue responses. Specifically, as observed in chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis, the mitochondria-endoplasmic reticulum (ER) crosstalk is disrupted by the inhaled toxicants such as the combustible and emerging electronic nicotine-delivery system (ENDS) tobacco products. Thus, the recent research efforts have focused on understanding how the mitochondria-ER dysfunctions and oxidative stress responses can be targeted to improve inflammatory and cellular dysfunctions associated with these pathologic illnesses that are exacerbated by viral infections. The present review assesses the importance of these redox signaling and cellular senescence pathways that describe the role of mitochondria and ER on the development and function of lung epithelial responses, highlighting the cause and effect associations that reflect the disease pathogenesis and possible intervention strategies.

Indexed as

Cellular SenescencePulmonary Disease, Chronic ObstructiveHumansLungMitochondriaOxidative StressCellular senescenceCigarette smokeCOPDDAMPsFibrosisMitochondrial dysfunctionROSUPR

Identifiers

PMID32037306
PMCPMC7251248
OpenAlexW3001036720

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.