Evidence map›Paper›PMID 34573330›Full record

ReviewGenes2021

Mitochondrial Dysfunction in Diseases, Longevity, and Treatment Resistance: Tuning Mitochondria Function as a Therapeutic Strategy.

Kazuo Tomita, Yoshikazu Kuwahara, Kento Igarashi, Mehryar Habibi Roudkenar, Amaneh Mohammadi Roushandeh, Akihiro Kurimasa, Tomoaki Sato

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Journal of dental sciences · 2026
    Article
  3. The dual-coding gene SLC35A4 protects against oxidative stress.Protein science : a publication of the Protein Society · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Furanoditerpenes fromACS chemical neuroscience · 2022
    Article
  15. SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022
    Review
  16. 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

7 authors at 3 institutions in 2 countries.

Kazuo TomitaDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Yoshikazu KuwaharaDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Kento IgarashiDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Mehryar Habibi RoudkenarDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Amaneh Mohammadi RoushandehDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Akihiro KurimasaDivision of Radiation Biology and Medicine, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1 Fukumuro, Sendai-City 983-8536, Miyagi, Japan.
Tomoaki SatoDepartment of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima-City 890-8544, Kagoshima, Japan.
Kagoshima University · JPGuilan University of Medical Sciences · IRTohoku Medical and Pharmaceutical University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are very important intracellular organelles because they have various functions. They produce ATP, are involved in cell signaling and cell death, and are a major source of reactive oxygen species (ROS). Mitochondria have their own DNA (mtDNA) and mutation of mtDNA or change the mtDNA copy numbers leads to disease, cancer chemo/radioresistance and aging including longevity. In this review, we discuss the mtDNA mutation, mitochondrial disease, longevity, and importance of mitochondrial dysfunction in cancer first. In the later part, we particularly focus on the role in cancer resistance and the mitochondrial condition such as mtDNA copy number, mitochondrial membrane potential, ROS levels, and ATP production. We suggest a therapeutic strategy employing mitochondrial transplantation (mtTP) for treatment-resistant cancer.

Indexed as

MutationAdenosine TriphosphateCell TransplantationDNA, MitochondrialHumansLongevityMitochondriaMitochondrial DiseasesNeoplasmsRadiation ToleranceAdenosine TriphosphateDNA, Mitochondrialcancer radioresistanceclinically relevant radioresistant (CRR) cellsmitochondriamitochondrial DNA

Identifiers

PMID34573330
PMCPMC8467098
OpenAlexW3198906953

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.