Evidence map›Paper›PMID 39184442›Full record

ArticleiScience2024

Astroglia proliferate upon the biogenesis of tunneling nanotubes via α-synuclein dependent transient nuclear translocation of focal adhesion kinase.

Abinaya Raghavan, Rachana Kashyap, P Sreedevi, Sneha Jos, Suchana Chatterjee, Ann Alex, Michelle Ninochka D'Souza, Mridhula Giridharan, Ravi Muddashetty, Ravi Manjithaya and 2 more

Abstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026
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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

12 authors.

Abinaya RaghavanManipal Institute of Regenerative Medicine, Bengaluru, Manipal Academy of Higher Education, Manipal, India.
Rachana KashyapManipal Institute of Regenerative Medicine, Bengaluru, Manipal Academy of Higher Education, Manipal, India.
P SreedeviAutophagy Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
Sneha JosDepartment of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India.
Suchana ChatterjeeManipal Institute of Regenerative Medicine, Bengaluru, Manipal Academy of Higher Education, Manipal, India.
Ann AlexManipal Institute of Regenerative Medicine, Bengaluru, Manipal Academy of Higher Education, Manipal, India.
Michelle Ninochka D'SouzaCentre for Brain Research, Indian Institute of Science, CV Raman Avenue, Bengaluru, India.
Mridhula GiridharanAutophagy Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
Ravi MuddashettyCentre for Brain Research, Indian Institute of Science, CV Raman Avenue, Bengaluru, India.
Ravi ManjithayaAutophagy Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
Sivaraman PadavattanDepartment of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India.
Sangeeta NathManipal Institute of Regenerative Medicine, Bengaluru, Manipal Academy of Higher Education, Manipal, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astroglia play crucial neuroprotective roles by internalizing pathogenic aggregates and facilitating their degradation. Here, we show that α-SYN protofibril-induced organelle toxicities and reactive oxygen species (ROS) cause premature cellular senescence in astrocytes and astrocyte-derived cancer cells, resulting in a transient increase in the biogenesis of tunneling nanotubes (TNTs). TNT-biogenesis and TNT-mediated cell-to-cell transfer lead to clearance of α-SYN-induced organelle toxicities, reduction in cellular ROS levels, and reversal of cellular senescence. Enhanced cell proliferation is seen in the post-recovered cells after recovering from α-SYN-induced organelle toxicities. Further, we show that α-SYN-induced senescence promotes the transient localization of focal adhesion kinase (FAK) in the nucleus. FAK-mediated regulation of Rho-associated kinases plays a significant role in the biogenesis of TNTs and their subsequent proliferation. Our study emphasizes that TNT biogenesis has a potential role in the clearance of α-SYN-induced cellular toxicities, the consequences of which cause enhanced proliferation in the post-recovered astroglia cells.

Indexed as

Biological sciencesCell biologyMolecular biologyNeuroscience

Identifiers

PMID39184442
PMCPMC11342280

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.