Evidence map›Paper›PMID 32110085›Full record

ReviewJournal of inflammation research2020

Mitochondrial Dynamic Dysfunction as a Main Triggering Factor for Inflammation Associated Chronic Non-Communicable Diseases.

Zeleke Geto, Meseret Derbew Molla, Feyissa Challa, Yohannes Belay, Tigist Getahun

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
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  5. Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 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

5 authors at 2 institutions in 1 country.

Zeleke GetoNational Reference Laboratory for Clinical Chemistry, Ethiopian Public Health Institute, Addis Ababa, Ethiopia.ORCID 0000-0001-8332-8885
Meseret Derbew MollaDepartment of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia.
Feyissa ChallaNational Reference Laboratory for Clinical Chemistry, Ethiopian Public Health Institute, Addis Ababa, Ethiopia.ORCID 0000-0002-2624-6661
Yohannes BelayNational Reference Laboratory for Hematology and Immunology, Ethiopian Public Health Institute, Addis Ababa, Ethiopia.
Tigist GetahunNational Reference Laboratory for Clinical Chemistry, Ethiopian Public Health Institute, Addis Ababa, Ethiopia.ORCID 0000-0001-6899-7247
Ethiopian Public Health Institute · ETUniversity of Gondar · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are organelles with highly dynamic ultrastructure maintained by flexible fusion and fission rates governed by Guanosine Triphosphatases (GTPases) dependent proteins. Balanced control of mitochondrial quality control is crucial for maintaining cellular energy and metabolic homeostasis; however, dysfunction of the dynamics of fusion and fission causes loss of integrity and functions with the accumulation of damaged mitochondria and mitochondrial deoxyribose nucleic acid (mtDNA) that can halt energy production and induce oxidative stress. Mitochondrial derived reactive oxygen species (ROS) can mediate redox signaling or, in excess, causing activation of inflammatory proteins and further exacerbate mitochondrial deterioration and oxidative stress. ROS have a deleterious effect on many cellular components, including lipids, proteins, both nuclear and mtDNA and cell membrane lipids producing the net result of the accumulation of damage associated molecular pattern (DAMPs) capable of activating pathogen recognition receptors (PRRs) on the surface and in the cytoplasm of immune cells. Chronic inflammation due to oxidative damage is thought to trigger numerous chronic diseases including cardiac, liver and kidney disorders, neurodegenerative diseases (Parkinson's disease and Alzheimer's disease), cardiovascular diseases/atherosclerosis, obesity, insulin resistance, and type 2 diabetes mellitus.

Indexed as

dynamicsinflammationmitochondrianon-communicable diseases

Identifiers

PMID32110085
PMCPMC7034420
OpenAlexW3005846825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.