Evidence map›Paper›PMID 35357640›Full record

ReviewInternational ophthalmology2022

Mesenchymal stem cells (MSCs) in Leber's hereditary optic neuropathy (LHON): a potential therapeutic approach for future.

Mohana Devi Subramaniam, Ruth Bright Chirayath, Mahalaxmi Iyer, Aswathy P Nair, Balachandar Vellingiri

Abstract readReview
PubMed Publisher
In one paragraph

Review in International ophthalmology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. 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

5 authors at 2 institutions in 1 country.

Mohana Devi SubramaniamSN ONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Chennai, 600 006, India. geneticmohana@gmail.com.
Ruth Bright ChirayathSN ONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Chennai, 600 006, India.
Mahalaxmi IyerSN ONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Chennai, 600 006, India.
Aswathy P NairSN ONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Chennai, 600 006, India.
Balachandar VellingiriDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, 641 046, India.
Oil and Natural Gas Corporation (India) · INBharathiar University · IN

Funding

Indian Council of Medical Research 2018-2786/CMB/Adhoc-BMS
6 · The paper itself

Abstract

backgroundOptic neuropathy has become a new typical syndromic multi-system disease that leads to optic atrophy. This review discusses potential treatments and advances of Leber's hereditary optic neuropathy (LHON), a sporadic genetic disorder. LHON is caused due to slight mutations in mitochondria leading to mitochondrial dysfunction, causing vision loss. There are no current significant treatments that have been proven to work for LHON.

methodsHowever, extensive review was carried out on capable studies that have shown potential treatment sensory systems and are being evaluated currently. Some of these studies are in clinical trials, whereas other ones are still being planned. Here, we focus more on treatment based on mesenchymal stem cells-mediated mitochondrial transfer via various techniques. We discuss different mitochondrial transfer modes and possible ways to understand the mitochondria transfer technique's phenotypic characteristics.

conclusionIt is clearly understood that transfer of healthy mitochondria from MSC to target cell would regulate the range of reactive oxygen species and ATP'S, which are majorly responsible for mutation upon irregulating. Therefore, mitochondrial transfer is suggested and discussed in this review with various aspects. The graphical abstract represents different means of mitochondrial transport like (a) Tunnelling nanotubules, (b) Extracellular vesicles, (c) Cell fusion and (d) Gap junctions. In (a) Tunnelling nanotubules, the signalling pathways TNF- α/TNF αip2 and NFkB/TNF αep2 are responsible for forming tunnels. Also, Miro protein acts as cargo for the transport of mitochondria with myosin's help in the presence of RhoGTPases [35]. In (b) Extracellular vesicles, the RhoA ARF6 contributes to Actin/Cytoskeletal rearrangement leading to the shedding of microvesicles. Coming to (c) Cell fusion when there is a high amount of ATP, the cells tend to fuse when in close proximity leading to the transfer of mitochondria via EFF-1/HAP2 [48]. In (d) Gap Junctions, Connexin43 is responsible for the intracellular channel in the presence of more ATP [86].

Indexed as

Mesenchymal Stem CellsOptic Atrophy, Hereditary, LeberAdenosine TriphosphateDNA, MitochondrialHumansMitochondriaMutationReactive Oxygen SpeciesAdenosine TriphosphateDNA, MitochondrialReactive Oxygen SpeciesGene therapyLeber’s hereditary optic neuropathyMesenchymal stem cellsMicro-vesicles-mediated transferMitochondrial transferTunnelling nanotubes

Identifiers

PMID35357640
OpenAlexW4220684028

What OpenQuestion holds

Textmetadata
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.