Evidence map›Paper›PMID 32032734›Full record

ArticleNeurobiology of disease2020

Dysregulated iron metabolism in C. elegans catp-6/ATP13A2 mutant impairs mitochondrial function.

Nikhita Anand, Angelina Holcom, Michael Broussalian, Minna Schmidt, Shankar J Chinta, Gordon J Lithgow, Julie K Andersen, Manish Chamoli

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Iron-deplete diet enhancesbioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Taurine deficiency as a driver of aging.Science (New York, N.Y.) · 2023
    Article
  13. Article
  14. ATP13A2 (PARK9) and basal ganglia function.Frontiers in neurology · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Nikhita AnandBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA.
Angelina HolcomBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA.
Michael BroussalianBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA.
Minna SchmidtBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA.
Shankar J ChintaBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA; Touro University California, Vallejo, USA.
Gordon J LithgowBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA.
Julie K AndersenBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA. Electronic address: JAndersen@buckinstitute.org.
Manish ChamoliBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, USA. Electronic address: MChamoli@buckinstitute.org.
Buck Institute for Research on Aging · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Potential role of lysosomal ATP13A2 in cellular iron homeostasisR21NS095758 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI ANDERSEN, JULIE KAY · 2016 to 2017
$534k
NIH HHS P40 OD010440NINDS NIH HHS R21 NS095758
6 · The paper itself

Abstract

Mutations in the human ATP13A2 gene are associated with an early-onset form of Parkinson's disease (PD) known as Kufor Rakeb Syndrome (KRS). Patients with KRS show increased iron deposition in the basal ganglia, suggesting iron toxicity-induced neurodegeneration as a potential pathogenesis associated with the ATP13A2 mutation. Previously we demonstrated that functional losses of ATP13A2 disrupt the lysosomes ability to store excess iron, leading to reduce survival of dopaminergic neuronal cells. To understand the possible mechanisms involved, we studied a Caenorhabditis elegans mutant defective in catp-6 function, an ortholog of human ATP13A2 gene. Here we show that catp-6 mutant worms have defective autophagy and lysosomal function, demonstrate characteristic PD phenotypes including reduced motor function and dysregulated iron metabolism. Additionally, these mutants have defective mitochondrial health, which is rescuable via iron chelation or mitophagy induction.

Indexed as

Adenosine TriphosphatasesAnimalsAutophagyCaenorhabditis elegansCaenorhabditis elegans ProteinsDopaminergic NeuronsHumansIronLysosomesMitochondriaMutationParkinson DiseaseParkinsonian DisordersProton-Translocating ATPasesAdenosine TriphosphatasesATP13A2 protein, humanCaenorhabditis elegans ProteinsCATP-6 protein, C elegansIronProton-Translocating ATPasesATP13A2Catp-6C. elegansIron chelationIron metabolismLysosomesMitochondrial functionParkinson's diseaseTFEBUrolithin A

Identifiers

PMID32032734
PMCPMC7150649
OpenAlexW3005147187

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.