Evidence map›Paper›PMID 31564441›Full record

ArticleCell metabolism2019

Miro1 Marks Parkinson's Disease Subset and Miro1 Reducer Rescues Neuron Loss in Parkinson's Models.

Chung-Han Hsieh, Li Li, Roeland Vanhauwaert, Kong T Nguyen, Mary D Davis, Guojun Bu, Zbigniew K Wszolek, Xinnan Wang

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
11.1field-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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. The MIRO1-BAX Complex Dictates Life and Death at the Mitochondrial Gate.bioRxiv : the preprint server for biology · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Molecular mechanisms of mitochondrial quality control.Translational neurodegeneration · 2025
    Review
  20. Review

37 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

8 authors at 3 institutions in 1 country.

Chung-Han HsiehDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Li LiDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Roeland VanhauwaertDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kong T NguyenAtomwise Inc., San Francisco, CA 94105, USA.
Mary D DavisDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Guojun BuDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Zbigniew K WszolekDepartment of Neurology, Mayo Clinic, Jacksonville, FL 32224, USA.
Xinnan WangDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: xinnanw@stanford.edu.
Stanford University · USMayo Clinic in Florida · USHealthwise · US

Funding

Stanford Center for Clinical & Translational Education and Research (Spectrum)UL1TR003142 · NCATS · STANFORD UNIVERSITY · PI O'HARA, RUTH M · 2019 to 2023
$45.0M
Working Memory in Parkinson Disease: A Cognitive & Systems Neuroscience ApproachP50AG047366 · NIA · STANFORD UNIVERSITY · PI HENDERSON, VICTOR · 2015 to 2019
$7.9M
Regulation of mitochondrial motility and mitophagy by LRRK2.R01NS089583 · NINDS · STANFORD UNIVERSITY · PI WANG, XINNAN · 2014 to 2018
$2.0M
A control center for mitochondrial navigation in neuronsR01GM143258 · NIGMS · STANFORD UNIVERSITY · PI WANG, XINNAN · 2021 to 2024
$1.5M
NCATS NIH HHS UL1 TR003142NIA NIH HHS P50 AG047366NIGMS NIH HHS R01 GM143258NINDS NIH HHS R01 NS089583
6 · The paper itself

Abstract

The identification of molecular targets and pharmacodynamic markers for Parkinson's disease (PD) will empower more effective clinical management and experimental therapies. Miro1 is localized on the mitochondrial surface and mediates mitochondrial motility. Miro1 is removed from depolarized mitochondria to facilitate their clearance via mitophagy. Here, we explore the clinical utility of Miro1 for detecting PD and for gauging potential treatments. We measure the Miro1 response to mitochondrial depolarization using biochemical assays in skin fibroblasts from a broad spectrum of PD patients and discover that more than 94% of the patients' fibroblast cell lines fail to remove Miro1 following depolarization. We identify a small molecule that can repair this defect of Miro1 in PD fibroblasts. Treating patient-derived neurons and fly models with this compound rescues the locomotor deficits and dopaminergic neurodegeneration. Our results indicate that tracking this Miro1 marker and engaging in Miro1-based therapies could open new avenues to personalized medicine.

Indexed as

Drosophila ProteinsMitochondrial ProteinsParkinson Diseaserho GTP-Binding ProteinsAdultAgedAnimalsAntiparkinson AgentsBiomarkersDrosophilaFemaleFibroblastsHEK293 CellsHumansInduced Pluripotent Stem CellsMaleAntiparkinson AgentsBiomarkersDrosophila ProteinsMiro protein, DrosophilaMitochondrial Proteinsrho GTP-Binding ProteinsRHOT1 protein, humanbiomarkerdietfibroblastflyiPSCMiro1mitochondriamitophagyneuronsParkinsonsmall moleculestherapy

Identifiers

PMID31564441
PMCPMC6893131
OpenAlexW2975042496

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.