Evidence map›Paper›PMID 37162686›Full record

ReviewNeurotoxicity research2023

Mitochondrial Dysfunction as a Signaling Target for Therapeutic Intervention in Major Neurodegenerative Disease.

Shubhada V Mangrulkar, Nitu L Wankhede, Mayur B Kale, Aman B Upaganlawar, Brijesh G Taksande, Milind J Umekar, Md Khalid Anwer, Hamad Ghaleb Dailah, Syam Mohan, Tapan Behl

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurotoxicity research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Modified TPP-MoSNeurology international · 2023
    Article
  18. 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

10 authors at 3 institutions in 2 countries.

Shubhada V MangrulkarSmt. Kishoritai Bhoyar College of Pharmacy, Kamptee, Nagpur, Maharashtra, India.
Nitu L WankhedeSmt. Shantabai Patil College of Diploma in Pharmacy, Kamptee, Nagpur, Maharashtra, India.
Mayur B KaleSmt. Kishoritai Bhoyar College of Pharmacy, Kamptee, Nagpur, Maharashtra, India.
Aman B UpaganlawarSNJB's Shriman Sureshdada Jain College of Pharmacy, Neminagar, Chandwad, Nasik, Maharashta, India.
Brijesh G TaksandeSmt. Kishoritai Bhoyar College of Pharmacy, Kamptee, Nagpur, Maharashtra, India.
Milind J UmekarSmt. Kishoritai Bhoyar College of Pharmacy, Kamptee, Nagpur, Maharashtra, India.
Md Khalid AnwerDepartment of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj, 16278, Saudi Arabia.
Hamad Ghaleb DailahResearch and Scientific Studies Unit, College of Nursing, Jazan University, Jazan, Saudi Arabia.
Syam MohanSubstance Abuse and Toxicology Research Center, Jazan University, Jazan, Saudi Arabia.
Tapan BehlSchool of Health Sciences and Technology, University of Petroleum and Energy Studies, Dehradun, Uttarakhand, India. tapanbehl31@gmail.com.
University of Petroleum and Energy Studies · INJazan University · SAPrince Sattam Bin Abdulaziz University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases (NDD) are incurable and the most prevalent cognitive and motor disorders of elderly. Mitochondria are essential for a wide range of cellular processes playing a pivotal role in a number of cellular functions like metabolism, intracellular signaling, apoptosis, and immunity. A plethora of evidence indicates the central role of mitochondrial functions in pathogenesis of many aging related NDD. Considering how mitochondria function in neurodegenerative diseases, oxidative stress, and mutations in mtDNA both contribute to aging. Many substantial reports suggested the involvement of numerous contributing factors including, mitochondrial dysfunction, oxidative stress, mitophagy, accumulation of somatic mtDNA mutations, compromised mitochondrial dynamics, and transport within axons in neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Amyotrophic Lateral Sclerosis. Therapies therefore target fundamental mitochondrial processes such as energy metabolism, free-radical generation, mitochondrial biogenesis, mitochondrial redox state, mitochondrial dynamics, mitochondrial protein synthesis, mitochondrial quality control, and metabolism hold great promise to develop pharmacological based therapies in NDD. By emphasizing the most efficient pharmacological strategies to target dysfunction of mitochondria in the treatment of neurodegenerative diseases, this review serves the scientific community engaged in translational medical science by focusing on the establishment of novel, mitochondria-targeted treatment strategies.

Indexed as

Neurodegenerative DiseasesAgedAgingDNA, MitochondrialHumansMitochondriaOxidative StressDNA, MitochondrialFissionFusionMitochondrial dysfunctionMitochondrial medicineMitochondrial quality controlOxidative stress

Identifiers

PMID37162686
OpenAlexW4376121364

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.