Evidence map›Paper›PMID 34768878›Full record

ReviewInternational journal of molecular sciences2021

Targetable Pathways for Alleviating Mitochondrial Dysfunction in Neurodegeneration of Metabolic and Non-Metabolic Diseases.

Lauren Elizabeth Millichap, Elisabetta Damiani, Luca Tiano, Iain P Hargreaves

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  20. IBRO neuroscience reports · 2022
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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

4 authors at 2 institutions in 2 countries.

Lauren Elizabeth MillichapDepartment of Life and Environmental Sciences, Polytechnic University of Marche, I-60131 Ancona, Italy.
Elisabetta DamianiDepartment of Life and Environmental Sciences, Polytechnic University of Marche, I-60131 Ancona, Italy.
Luca TianoDepartment of Life and Environmental Sciences, Polytechnic University of Marche, I-60131 Ancona, Italy.ORCID 0000-0002-7519-7106
Iain P HargreavesSchool of Pharmacy, Liverpool John Moores University, Liverpool L3 5UA, UK.
Marche Polytechnic University · ITLiverpool John Moores University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many neurodegenerative and inherited metabolic diseases frequently compromise nervous system function, and mitochondrial dysfunction and oxidative stress have been implicated as key events leading to neurodegeneration. Mitochondria are essential for neuronal function; however, these organelles are major sources of endogenous reactive oxygen species and are vulnerable targets for oxidative stress-induced damage. The brain is very susceptible to oxidative damage due to its high metabolic demand and low antioxidant defence systems, therefore minimal imbalances in the redox state can result in an oxidative environment that favours tissue damage and activates neuroinflammatory processes. Mitochondrial-associated molecular pathways are often compromised in the pathophysiology of neurodegeneration, including the parkin/PINK1, Nrf2, PGC1α, and PPARγ pathways. Impairments to these signalling pathways consequently effect the removal of dysfunctional mitochondria, which has been suggested as contributing to the development of neurodegeneration. Mitochondrial dysfunction prevention has become an attractive therapeutic target, and there are several molecular pathways that can be pharmacologically targeted to remove damaged mitochondria by inducing mitochondrial biogenesis or mitophagy, as well as increasing the antioxidant capacity of the brain, in order to alleviate mitochondrial dysfunction and prevent the development and progression of neurodegeneration in these disorders. Compounds such as natural polyphenolic compounds, bioactive quinones, and Nrf2 activators have been reported in the literature as novel therapeutic candidates capable of targeting defective mitochondrial pathways in order to improve mitochondrial function and reduce the severity of neurodegeneration in these disorders.

Indexed as

AnimalsAntioxidantsHumansMetabolic DiseasesMitochondriaMitophagyNeurodegenerative DiseasesNeuronsOxidation-ReductionOxidative StressReactive Oxygen SpeciesAntioxidantsReactive Oxygen Speciesantioxidant defenseslysosomal storage disordersmethylmalonic acidaemiamitochondrial biogenesismitochondrial dysfunctionmitophagyneurodegenerationoxidative stressParkinson’s diseasetherapeutics

Identifiers

PMID34768878
PMCPMC8583882
OpenAlexW3211144031

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.