Evidence map›Paper›PMID 38910425›Full record

ReviewCurrent drug targets2024

Targeted Treatment Strategies for Mitochondria Dysfunction: Correlation with Neurological Disorders.

Rishav Sharma, Rishabha Malviya, Saurabh Srivastava, Irfan Ahmad, Safia Obaidur Rab, Prerna Uniyal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. [Research progress of metalloporphyrin against neurodegene-rative diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    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

6 authors.

Rishav SharmaDepartment of Pharmacy, School of Medical and Allied Sciences, Galgotias University, Greater Noida, U.P., India.
Rishabha MalviyaDepartment of Pharmacy, School of Medical and Allied Sciences, Galgotias University, Greater Noida, U.P., India.ORCID 0000-0003-2874-6149
Saurabh SrivastavaSchool of Pharmacy, KPJ Healthcare University College (KPJUC), Nilai, Malaysia.
Irfan AhmadDepartment of Clinical Laboratory Sciences, College of Applied Medical Science, King Khalid University, Abha, Saudi Arabia.
Safia Obaidur RabDepartment of Clinical Laboratory Sciences, College of Applied Medical Science, King Khalid University, Abha, Saudi Arabia.
Prerna UniyalSchool of Pharmacy, Graphic Era Hill University, Dehradun, India.

Funding

King Khalid University grant number RGP.02/557/44.
6 · The paper itself

Abstract

Mitochondria are an essential intracellular organelle for medication targeting and delivery since they seem to create energy and conduct many other cellular tasks, and mitochondrial dysfunctions and malfunctions lead to many illnesses. Many initiatives have been taken to detect, diagnose, and image mitochondrial abnormalities, and to transport and accumulate medicines precisely to mitochondria, all because of special mitochondrial aspects of the pathophysiology of cancer. In addition to the negative membrane potential and paradoxical mitochondrial dynamics, they include high temperatures, high levels of reactive oxygen species, high levels of glutathione, and high temperatures. Neurodegenerative diseases represent a broad spectrum of debilitating illnesses. They are linked to the loss of certain groups of neurons based on an individual's physiology or anatomy. The mitochondria in a cell are generally accepted as the authority with respect to ATP production. Disruption of this system is linked to several cellular physiological issues. The development of neurodegenerative disorders has been linked to mitochondrial malfunction, according to pathophysiological studies. There seems to be substantial evidence connecting mitochondrial dysfunction and oxidative stress to the development of neurodegenerative disorders. It has been extensively observed that mitochondrial malfunction triggers autophagy, which plays a role in neurodegenerative disorders. In addition, excitotoxicity and mitochondrial dysfunction have been linked to the development of neurodegenerative disorders. The pathophysiology of neurodegenerative illnesses has been linked to increased apoptosis and necrosis, as well as mitochondrial malfunction. A variety of synthetic and natural treatments have shown efficacy in treating neurodegenerative illnesses caused by mitochondrial failure. Neurodegenerative illnesses can be effectively treated with existing drugs that target mitochondria, although their precise formulations are poorly understood. Therefore, there is an immediate need to focus on creating drug delivery methods specifically targeted at mitochondria in the treatment and diagnosis of neurodegenerative disorders.

Indexed as

MitochondriaNeurodegenerative DiseasesAnimalsAutophagyDrug Delivery SystemsHumansMitochondrial DiseasesMolecular Targeted TherapyNervous System DiseasesOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesAlzheimer’s diseasecytochrome.Mitochondrial dysfunctionneurodegenerative diseasesROStargeted therapy

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.