Evidence map›Paper›PMID 39466510›Full record

ReviewJournal of molecular neuroscience : MN2024

Signaling Pathways Concerning Mitochondrial Dysfunction: Implications in Neurodegeneration and Possible Molecular Targets.

Yati Sharma, Jeetendra Kumar Gupta, M Arockia Babu, Sumitra Singh, Rakesh K Sindhu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular neuroscience : MN, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. 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

5 authors.

Yati SharmaInstitute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, 281406, India.
Jeetendra Kumar GuptaInstitute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, 281406, India.
M Arockia BabuInstitute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, 281406, India.
Sumitra SinghDepartment of Pharmaceutical Sciences, Guru Jambheshwar University of Science and Technology, Hisar, Haryana, 125001, India.
Rakesh K SindhuSchool of Pharmacy, Sharda University, Gautam Buddha Nagar, Greater Noida, Uttar Paresdh, 201310, India. drrakeshksindhu@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrion is an important organelle present in our cells responsible for meeting energy requirements. All higher organisms rely on efficient mitochondrial bioenergetic machinery to sustain life. No other respiratory process can produce as much power as generated by mitochondria in the form of ATPs. This review is written in order to get an insight into the magnificent working of mitochondrion and its implications in cellular homeostasis, bioenergetics, redox, calcium signaling, and cell death. However, if this machinery gets faulty, it may lead to several disease states. Mitochondrial dysfunctioning is of growing concern today as it is seen in the pathogenesis of several diseases which includes neurodegenerative disorders, cardiovascular disorders, diabetes mellitus, skeletal muscle defects, liver diseases, and so on. To cover all these aspects is beyond the scope of this article; hence, our study is restricted to neurodegenerative disorders only. Moreover, faulty functioning of this organelle can be one of the causes of early ageing in individuals. This review emphasizes mutations in the mitochondrial DNA, defects in oxidative phosphorylation, generation of ROS, and apoptosis. Researchers have looked into new approaches that might be able to control mitochondrial failure and show a lot of promise as treatments.

Indexed as

MitochondriaNeurodegenerative DiseasesAnimalsDNA, MitochondrialHumansReactive Oxygen SpeciesSignal TransductionDNA, MitochondrialReactive Oxygen SpeciesMitochondrial dysfunctionNeurodegenerationNeurotoxicityOxidative stress

Identifiers

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.