Evidence map›Paper›PMID 32289315›Full record

ReviewExperimental neurology2020

Mitochondrial biogenesis as a therapeutic target for traumatic and neurodegenerative CNS diseases.

Epiphani C Simmons, Natalie E Scholpa, Rick G Schnellmann

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
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  8. The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025
    Review
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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

3 authors at 1 institution in 1 country.

Epiphani C SimmonsDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States of America; Department of Neurosciences, College of Medicine, University of Arizona, Tucson, AZ, United States of America. Electronic address: esimmons@pharmacy.arizona.edu.
Natalie E ScholpaDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States of America. Electronic address: scholpa@pharmacy.arizona.edu.
Rick G SchnellmannDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States of America; Department of Neurosciences, College of Medicine, University of Arizona, Tucson, AZ, United States of America; Southern Arizona VA Health Care System, Tucson, AZ, United States of America; Southwest Environmental Health Science Center, University of Arizona, Tucson, AZ, United States of America; Center for Innovation in Brain Science, University of Arizona, Tucson, AZ, United States of America. Electronic address: schnell@pharmacy.arizona.edu.
University of Arizona · US

Funding

Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Mitochondrial Biogenesis Promotes Recovery From Oxidant InjuryR01GM084147 · NIGMS · UNIVERSITY OF ARIZONA · PI SCHNELLMANN, RICK G · 2008 to 2016
$2.4M
Translational research in Alzheimer’s Disease and Related Dementias (TRADD)T32AG061897 · NIA · UNIVERSITY OF ARIZONA · PI BRINTON, ROBERTA EILEEN · 2018 to 2022
$1.3M
5-HT Stimulation of Mitochondrial Biogenesis and Acute Kidney InjuryI01BX000851 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI SCHNELLMANN, RICK G · 2011 to 2025
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5-HT1F receptor agonism as a novel therapeutic strategy following spinal cord injuryI01BX004868 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI SCHNELLMANN, RICK G · 2020 to 2023
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BLRD VA I01 BX000851BLRD VA I01 BX004868NIAID NIH HHS U19 AI068021NIA NIH HHS T32 AG061897NIGMS NIH HHS R01 GM084147
6 · The paper itself

Abstract

Central nervous system (CNS) diseases, both traumatic and neurodegenerative, are characterized by impaired mitochondrial bioenergetics and often disturbed mitochondrial dynamics. The dysregulation observed in these pathologies leads to defective respiratory chain function and reduced ATP production, thereby promoting neuronal death. As such, attenuation of mitochondrial dysfunction through induction of mitochondrial biogenesis (MB) is a promising, though still underexplored, therapeutic strategy. MB is a multifaceted process involving the integration of highly regulated transcriptional events, lipid membrane and protein synthesis/assembly and replication of mtDNA. Several nuclear transcription factors promote the expression of genes involved in oxidative phosphorylation, mitochondrial import and export systems, antioxidant defense and mitochondrial gene transcription. Of these, the nuclear-encoded peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is the most commonly studied and is widely accepted as the 'master regulator' of MB. Several recent preclinical studies document that reestablishment of mitochondrial homeostasis through increased MB results in inhibited injury progression and increased functional recovery. This perspective will briefly review the role of mitochondrial dysfunction in the propagation of CNS diseases, while also describing current research strategies that mediate mitochondrial dysfunction and compounds that induce MB for the treatment of acute and chronic neuropathologies.

Indexed as

Organelle BiogenesisAnimalsBrain Injuries, TraumaticHumansMitochondriaNeurodegenerative DiseasesSpinal Cord InjuriesAlzheimer’s diseaseMitochondrial biogenesisMitochondrial dynamicsMitochondrial dysfunctionMitophagyNeuroinflammationParkinson’s diseaseSpinal cord injuryStrokeTraumatic brain injury

Identifiers

PMID32289315
PMCPMC7735537
OpenAlexW3015997282

What OpenQuestion holds

Textmetadata
LicenceTDM
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.