Evidence map›Paper›PMID 36111770›Full record

ReviewCurrent neuropharmacology2023

Boosting Mitochondrial Potential: An Imperative Therapeutic Intervention in Amyotrophic Lateral Sclerosis.

Swati Dhasmana, Anupam Dhasmana, Sudhir Kotnala, Varsha Mangtani, Acharan S Narula, Shafiul Haque, Meena Jaggi, Murali M Yallapu, Subhash C Chauhan

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current neuropharmacology, 2023. 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
0.9field-weighted citation impact, top 25% 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, 7 citations in OpenAlex.

  1. Article
  2. Trimetazidine Improves Mitochondrial Dysfunction in SOD1International journal of molecular sciences · 2024
    Article
  3. Article
  4. Article
  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

9 authors at 2 institutions in 4 countries.

Swati DhasmanaDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Anupam DhasmanaDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Sudhir KotnalaDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Varsha MangtaniDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Acharan S NarulaNarula Research LLC, 107 Boulder Bluff, Chapel Hill, North Carolina, NC 27516, USA.
Shafiul HaqueResearch and Scientific Studies Unit, College of Nursing and Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Meena JaggiDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Murali M YallapuDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
Subhash C ChauhanDepartment of Immunology & Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, Texas, TX, USA.
The University of Texas Rio Grande Valley · USJazan University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmyotrophic Lateral Sclerosis (ALS) is a progressive and terminal neurodegenerative disorder. Mitochondrial dysfunction, imbalance of cellular bioenergetics, electron chain transportation and calcium homeostasis are deeply associated with the progression of this disease. Impaired mitochondrial functions are crucial in rapid neurodegeneration. The mitochondria of ALS patients are associated with deregulated Ca

objectiveThe aim of this review is to brief the latest developments in the understanding of mitochondrial pathogenesis in ALS and emphasize the restorative capacity of therapeutic candidates.

resultsIn ALS, mitochondrial dysfunction is a well-known phenomenon. Various therapies targeted towards mitochondrial dysfunction aim at decreasing ROS generation, increasing mitochondrial biogenesis, and inhibiting apoptotic pathways. Some of the therapies briefed in this review may be categorized as synthetic, natural compounds, genetic materials, and cellular therapies.

conclusionThe overarching goals of mitochondrial therapies in ALS are to benefit ALS patients by slowing down the disease progression and prolonging overall survival. Despite various therapeutic approaches, there are many hurdles in the development of a successful therapy due to the multifaceted nature of mitochondrial dysfunction and ALS progression. Intensive research is required to precisely elucidate the molecular pathways involved in the progression of mitochondrial dysfunctions that ultimately lead to ALS. Because of the multifactorial nature of ALS, a combination therapy approach may hold the key to cure and treat ALS in the future.

Indexed as

Amyotrophic Lateral SclerosisCalciumHumansMitochondriaOxidative StressReactive Oxygen SpeciesCalciumReactive Oxygen SpeciesALSexcitotoxicitymitochondrial biogenesismitochondrial dysfunctionmitochondrial reactivationneurodegenerationROS in ALS

Identifiers

PMID36111770
PMCPMC10286590
OpenAlexW4296037210

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.