Evidence map›Paper›PMID 29379409›Full record

ArticleFrontiers in neuroscience2017

Parkinson's Disease Skin Fibroblasts Display Signature Alterations in Growth, Redox Homeostasis, Mitochondrial Function, and Autophagy.

Joji M Y Teves, Vedanshi Bhargava, Konner R Kirwan, Mandi J Corenblum, Rebecca Justiniano, Georg T Wondrak, Annadurai Anandhan, Andrew J Flores, David A Schipper, Zain Khalpey and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.5field-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

41 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. In Vivo UV-Induced Fluorescence Spectroscopy of Skin in Parkinson's Disease.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2025
    Article
  6. Article
  7. Review
  8. YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.International journal of molecular sciences · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
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  15. Article
  16. Review
  17. A heterozygous p.S143P mutation inFrontiers in cell and developmental biology · 2022
    Article
  18. Review
  19. Article
  20. Article
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

14 authors at 1 institution in 1 country.

Joji M Y TevesGraduate Interdisciplinary Program in Applied Biosciences, University of Arizona, Tucson, AZ, United States.
Vedanshi BhargavaNeuroscience and Cognitive Science Undergraduate Program, Undergraduate Biology Research Program, University of Arizona, Tucson, AZ, United States.
Konner R KirwanNeuroscience and Cognitive Science Undergraduate Program, Undergraduate Biology Research Program, University of Arizona, Tucson, AZ, United States.
Mandi J CorenblumDepartment of Neurology, University of Arizona, Tucson, AZ, United States.
Rebecca JustinianoPharmacology and Toxicology, University of Arizona, Tucson, AZ, United States.
Georg T WondrakPharmacology and Toxicology, University of Arizona, Tucson, AZ, United States.
Annadurai AnandhanDepartment of Neurology, University of Arizona, Tucson, AZ, United States.
Andrew J FloresGraduate Interdisciplinary Program in Physiological Sciences, University of Arizona, Tucson, AZ, United States.
David A SchipperDepartment of Surgery, University of Arizona, Tucson, AZ, United States.
Zain KhalpeyDepartment of Surgery, University of Arizona, Tucson, AZ, United States.
James E SlighDepartment of Medicine, University of Arizona, Tucson, AZ, United States.
Clara Curiel-LewandrowskiDepartment of Medicine, University of Arizona, Tucson, AZ, United States.
Scott J ShermanDepartment of Neurology, University of Arizona, Tucson, AZ, United States.
Lalitha MadhavanDepartment of Neurology, University of Arizona, Tucson, AZ, United States.
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
NCI NIH HHS P30 CA023074NIEHS NIH HHS P30 ES006694NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

The discovery of biomarkers for Parkinson's disease (PD) is challenging due to the heterogeneous nature of this disorder, and a poor correlation between the underlying pathology and the clinically expressed phenotype. An ideal biomarker would inform on PD-relevant pathological changes via an easily assayed biological characteristic, which reliably tracks clinical symptoms. Human dermal (skin) fibroblasts are accessible peripheral cells that constitute a patient-specific system, which potentially recapitulates the PD chronological and epigenetic aging history. Here, we compared primary skin fibroblasts obtained from individuals diagnosed with late-onset sporadic PD, and healthy age-matched controls. These fibroblasts were studied from fundamental viewpoints of growth and morphology, as well as redox, mitochondrial, and autophagic function. It was observed that fibroblasts from PD subjects had higher growth rates, and appeared distinctly different in terms of morphology and spatial organization in culture, compared to control cells. It was also found that the PD fibroblasts exhibited significantly compromised mitochondrial structure and function when assessed via morphological and oxidative phosphorylation assays. Additionally, a striking increase in baseline macroautophagy levels was seen in cells from PD subjects. Exposure of the skin fibroblasts to physiologically relevant stress, specifically ultraviolet irradiation (UVA), further exaggerated the autophagic dysfunction in the PD cells. Moreover, the PD fibroblasts accumulated higher levels of reactive oxygen species (ROS) coupled with lower cell viability upon UVA treatment. In essence, these studies highlight primary skin fibroblasts as a patient-relevant model that captures fundamental PD molecular mechanisms, and supports their potential utility to develop diagnostic and prognostic biomarkers for the disease.

Indexed as

autophagyhuman dermal fibroblastsmitochondrial functionoxidative stressParkinson's diseasesporadicUVA irradiation

Identifiers

PMID29379409
PMCPMC5770791
OpenAlexW2784329444

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.