Evidence map›Paper›PMID 33079380›Full record

ReviewJournal of thrombosis and thrombolysis2021

Mitochondria and chronic effects of cancer therapeutics: The clinical implications.

Abishai Dominic, Dale Hamilton, Jun-Ichi Abe

Open access · greenAbstract readReview
In one paragraph

Review in Journal of thrombosis and thrombolysis, 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
1.6field-weighted citation impact, top 17% 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, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Observational
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  7. Article
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  11. Article
  12. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. 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

3 authors at 3 institutions in 1 country.

Abishai DominicDepartment of Cardiovascular Sciences, Center for Cardiovascular Regeneration, Houston Methodist Research Institute, Houston, TX, USA.
Dale HamiltonDepartment of Medicine, Center for Bioenergetics Houston Methodist Research Institute, Houston, TX, USA.
Jun-Ichi AbeDepartment of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. jabe@mdanderson.org.ORCID http://orcid.org/0000-0001-7439-7774
Houston Methodist · USTexas A&M Health Science Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

PAR 13-233 cART accelerates vascular aging in HIV infected subjectsR01HL123346 · NHLBI · UNIVERSITY OF ROCHESTER · PI ABE, JUN-ICHI, MAGGIRWAR, SANJAY B. · 2014 to 2018
$3.7M
Pathological flow-induced endothelial damage and plaque erosionR01HL149303 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABE, JUN-ICHI, COOKE, JOHN P · 2019 to 2022
$3.2M
Mitigating radiation-induced cardiovascular disease by inhibiting premature agingU01AI156921 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABE, JUN-ICHI · 2020 to 2024
$2.5M
A Novel Role for MAGI1 in regulating non-canonical LATS signaling and atherosclerotic plaque formationR01HL134740 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LE, NHAT-TU · 2017 to 2021
$2.0M
Disturbed flow-induced TERF2IP post-translational modifications and atherosclerosis.R01HL130193 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABE, JUN-ICHI · 2016 to 2019
$2.0M
Cancer Prevention and Research Institute of Texas RP190256National Institute of Allergy and Infectious Diseases U01AI156921NHLBI NIH HHS HL134740NHLBI NIH HHS HL149303NHLBI NIH HHS R01 HL123346NHLBI NIH HHS R01 HL130193NHLBI NIH HHS R01 HL134740NHLBI NIH HHS R01 HL149303NIAID NIH HHS U01 AI156921
6 · The paper itself

Abstract

One of the major mechanisms of action of chemo-radiation is to induce cellular senescence, which exerts crucial roles in age-related pathology. The concept of senescence is evolved, and the novel understanding of senescence-associated reprogramming/stemness has emerged. This new concept emphasizes senescence as not only cell cycle arrest but describes that subsets of senescent cells induced by chemotherapy can re-enter cell cycles, proliferate rapidly, and acquire "stemness" status. Cancer therapeutics, including chemo-radiation triggers toxicity effects through damaging mitochondria, primarily through the upregulation of mtROS production leading to subsequent mtDNA and telomeric DNA damage elicitng DNA damage responses (DDR). The ultimate goal of this review is to highlight the new concept of senescence-associated stemness that is induced by cancer treatment and its adverse effects on the vascular system. We will describe how chemo-radiation exerts toxicity effects by simultaneously producing reactive oxygen species in mitochondria and promoting DDR in the nucleus. We discuss the potential of clinical targeting poly (ADP-ribose) polymerase which might prevent downstream mitochondrial dysfunction and confer protection to cancer survivors. Overall we emphasize the importance of recognizing the consequences of cardio-toxic effects of several cancer treatments and therefore developing personalized therapeutic approaches to screen for inflammatory and cardiac testing for better patient survival.

Indexed as

MitochondriaNeoplasmsCellular SenescenceDNA, MitochondrialHumansReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID33079380
PMCPMC8055726
OpenAlexW3092691797

What OpenQuestion holds

Textmetadata
LicenceTDM
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.