Evidence map›Paper›PMID 35626724›Full record

ReviewCells2022

Alterations of Mitochondrial Network by Cigarette Smoking and E-Cigarette Vaping.

Manasa Kanithi, Sunil Junapudi, Syed Islamuddin Shah, Alavala Matta Reddy, Ghanim Ullah, Bojjibabu Chidipi

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Developmental nicotine exposure alters cardiovascular structure and function in neonatal and juvenile rats.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  11. Review
  12. Review
  13. Nicotine affects mitochondrial structure and function in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  14. Article
  15. Impact ofFrontiers in pharmacology · 2023
    Article
  16. 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

6 authors at 3 institutions in 2 countries.

Manasa KanithiCollege of Osteopathic Medicine, Michigan State University, East Lansing, MI 48824, USA.
Sunil JunapudiDepartment of Pharmaceutical Chemistry, Geethanjali College of Pharmacy, Cherryal, Keesara, Medchalmalkajgiri District, Hyderabad 501301, India.
Syed Islamuddin ShahDepartment of Physics, University of South Florida, Tampa, FL 33620, USA.
Alavala Matta ReddyDepartment of Zoology, School of Life and Health Sciences, Adikavi Nannaya University, Rajahmundry 533296, India.ORCID 0000-0002-6955-2650
Ghanim UllahDepartment of Physics, University of South Florida, Tampa, FL 33620, USA.ORCID 0000-0002-3716-8742
Bojjibabu ChidipiMorsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.ORCID 0000-0003-4107-1668
University of South Florida · USAdikavi Nannaya University · INMichigan State University · US

Funding

A multi-scale data-driven model of the Abeta pore function and Ca2+ toxicity in Alzheimer's diseaseR01AG053988 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI DEMURO, ANGELO, ULLAH, GHANIM · 2016 to 2020
$2.1M
NIA NIH HHS R01 AG053988
6 · The paper itself

Abstract

Toxins present in cigarette and e-cigarette smoke constitute a significant cause of illnesses and are known to have fatal health impacts. Specific mechanisms by which toxins present in smoke impair cell repair are still being researched and are of prime interest for developing more effective treatments. Current literature suggests toxins present in cigarette smoke and aerosolized e-vapor trigger abnormal intercellular responses, damage mitochondrial function, and consequently disrupt the homeostasis of the organelle's biochemical processes by increasing reactive oxidative species. Increased oxidative stress sets off a cascade of molecular events, disrupting optimal mitochondrial morphology and homeostasis. Furthermore, smoking-induced oxidative stress may also amalgamate with other health factors to contribute to various pathophysiological processes. An increasing number of studies show that toxins may affect mitochondria even through exposure to secondhand or thirdhand smoke. This review assesses the impact of toxins present in tobacco smoke and e-vapor on mitochondrial health, networking, and critical structural processes, including mitochondria fission, fusion, hyper-fusion, fragmentation, and mitophagy. The efforts are focused on discussing current evidence linking toxins present in first, second, and thirdhand smoke to mitochondrial dysfunction.

Indexed as

Cigarette SmokingElectronic Nicotine Delivery SystemsTobacco Smoke PollutionVapingMitochondriaNicotianaTobacco Smoke Pollutioncigarette smokinge-cigarette smokingfissionfusionmitochondria

Identifiers

PMID35626724
PMCPMC9139349
OpenAlexW4280517466

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.