Evidence map›Paper›PMID 33404982›Full record

ArticleMolecular neurobiology2021

Exosome Release Is Modulated by the Mitochondrial-Lysosomal Crosstalk in Parkinson's Disease Stress Conditions.

Fatema Currim, Jyoti Singh, Anjali Shinde, Dhruv Gohel, Milton Roy, Kritarth Singh, Shatakshi Shukla, Minal Mane, Hitesh Vasiyani, Rajesh Singh

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Fatema CurrimDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Jyoti SinghDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Anjali ShindeDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Dhruv GohelDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Milton RoyDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Kritarth SinghDepartment of Cell and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK.
Shatakshi ShuklaDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Minal ManeDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Hitesh VasiyaniDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India.
Rajesh SinghDepartment of Biochemistry, Faculty of Science, The MS University of Baroda, Vadodara, Gujarat, 390002, India. singhraj1975@gmail.com.ORCID http://orcid.org/0000-0002-3734-4662
Maharaja Sayajirao University of Baroda · INUniversity College London · GB

Funding

Department of Biotechnology , Ministry of Science and Technology BT/PR19937/MED/122/17/2016
6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta region of the brain. The main pathological hallmark involves cytoplasmic inclusions of α-synuclein and mitochondrial dysfunction, which is observed in other part of the central nervous system other than SN suggesting the spread of pathogenesis to bystander neurons. The inter-neuronal communication through exosomes may play an important role in the spread of the disease; however, the mechanisms are not well elucidated. Mitochondria and its role in inter-organellar crosstalk with multivesicular body (MVB) and lysosome and its role in modulation of exosome release in PD is not well understood. In the current study, we investigated the mitochondria-lysosome crosstalk modulating the exosome release in neuronal and glial cells. We observed that PD stress showed enhanced release of exosomes in dopaminergic neurons and glial cells. The PD stress condition in these cells showed fragmented network and mitochondrial dysfunction which further leads to functional deficit of lysosomes and hence inhibition of autophagy flux. Neuronal and glial cells treated with rapamycin showed enhanced autophagy and inhibited the exosomal release. The results here suggest that maintenance of mitochondrial function is important for the lysosomal function and hence exosomal release which is important for the pathogenesis of PD.

Indexed as

Stress, PhysiologicalAutophagyCell Line, TumorExosomesHumansLysosomesMitochondriaParkinson DiseaseSirolimusSirolimusExosome releaseMitochondrial dysfunctionsMitochondria-lysosome crosstalkParkinson’s disease

Identifiers

PMID33404982
OpenAlexW3119427943

What OpenQuestion holds

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Registered trials

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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.