Evidence map›Paper›PMID 33640250›Full record

ReviewTrends in endocrinology and metabolism: TEM2021

Cardiolipin, Mitochondria, and Neurological Disease.

Micol Falabella, Hilary J Vernon, Michael G Hanna, Steven M Claypool, Robert D S Pitceathly

Open access · hybridAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
14.0field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 253 citations in OpenAlex.

  1. Article
  2. Cross-species evidence for cardiolipin remodeling in neonatal hypoxic-ischemic encephalopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  16. Alkyltriphenylphosphonium Binding to Cardiolipin Triggers Oncosis in Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Article

86 more citing papers are in PubMed but not listed here.

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 2 countries.

Micol FalabellaDepartment of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Hilary J VernonDepartment of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michael G HannaDepartment of Neuromuscular Diseases, University College London Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK.
Steven M ClaypoolDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Robert D S PitceathlyDepartment of Neuromuscular Diseases, University College London Queen Square Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK. Electronic address: r.pitceathly@ucl.ac.uk.
National Hospital for Neurology and Neurosurgery · GBJohns Hopkins University · US

Funding

Medical Research Council MR/S002065/1
6 · The paper itself

Abstract

Over the past decade, it has become clear that lipid homeostasis is central to cellular metabolism. Lipids are particularly abundant in the central nervous system (CNS) where they modulate membrane fluidity, electric signal transduction, and synaptic stabilization. Abnormal lipid profiles reported in Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and traumatic brain injury (TBI), are further support for the importance of lipid metablism in the nervous system. Cardiolipin (CL), a mitochondria-exclusive phospholipid, has recently emerged as a focus of neurodegenerative disease research. Aberrant CL content, structure, and localization are linked to impaired neurogenesis and neuronal dysfunction, contributing to aging and the pathogenesis of several neurodegenerative diseases, such as AD and PD. Furthermore, the highly tissue-specific acyl chain composition of CL confers it significant potential as a biomarker to diagnose and monitor the progression in several neurological diseases. CL also represents a potential target for pharmacological strategies aimed at treating neurodegeneration. Given the equipoise that currently exists between CL metabolism, mitochondrial function, and neurological disease, we review the role of CL in nervous system physiology and monogenic and neurodegenerative disease pathophysiology, in addition to its potential application as a biomarker and pharmacological target.

Indexed as

CardiolipinsMitochondriaNeurodegenerative DiseasesCentral Nervous SystemHumansNeuronsCardiolipinscardiolipinlipidsmitochondriamitochondrial diseasenervous systemneurodegeneration

Identifiers

PMID33640250
PMCPMC8277580
OpenAlexW3133026938

What Socratic 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 Socratic graph.