Evidence map›Paper›PMID 33110473›Full record

ReviewOxidative medicine and cellular longevity2020

Possible Susceptibility Genes for Intervention against Chemotherapy-Induced Cardiotoxicity.

Xinyu Yang, Guoping Li, Tao Yang, Manke Guan, Na An, Fan Yang, Qianqian Dai, Changming Zhong, Changyong Luo, Yonghong Gao and 3 more

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  14. Pharmaceutics · 2021
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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

13 authors at 4 institutions in 2 countries.

Xinyu Yang *Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
Guoping Li *Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Tao YangKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Manke GuanKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Na AnGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
Fan YangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
Qianqian DaiKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Changming ZhongKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Changyong LuoBeijing University of Chinese Medicine, Beijing 100029, China.
Yonghong GaoKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.ORCID https://orcid.org/0000-0002-3771-3528
Saumya DasCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.ORCID https://orcid.org/0000-0002-4521-4606
Yanwei XingGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.ORCID https://orcid.org/0000-0002-1392-9738
Hongcai ShangKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.ORCID https://orcid.org/0000-0002-6603-5666
Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNHarvard University · USBeijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent therapeutic advances have significantly improved the short- and long-term survival rates in patients with heart disease and cancer. Survival in cancer patients may, however, be accompanied by disadvantages, namely, increased rates of cardiovascular events. Chemotherapy-related cardiac dysfunction is an important side effect of anticancer therapy. While advances in cancer treatment have increased patient survival, treatments are associated with cardiovascular complications, including heart failure (HF), arrhythmias, cardiac ischemia, valve disease, pericarditis, and fibrosis of the pericardium and myocardium. The molecular mechanisms of cardiotoxicity caused by cancer treatment have not yet been elucidated, and they may be both varied and complex. By identifying the functional genetic variations responsible for this toxicity, we may be able to improve our understanding of the potential mechanisms and pathways of treatment, paving the way for the development of new therapies to target these toxicities. Data from studies on genetic defects and pharmacological interventions have suggested that many molecules, primarily those regulating oxidative stress, inflammation, autophagy, apoptosis, and metabolism, contribute to the pathogenesis of cardiotoxicity induced by cancer treatment. Here, we review the progress of genetic research in illuminating the molecular mechanisms of cancer treatment-mediated cardiotoxicity and provide insights for the research and development of new therapies to treat or even prevent cardiotoxicity in patients undergoing cancer treatment. The current evidence is not clear about the role of pharmacogenomic screening of susceptible genes. Further studies need to done in chemotherapy-induced cardiotoxicity.

Indexed as

Antineoplastic AgentsCardiotoxicityHeart DiseasesHumansMicroRNAsNADPH OxidasesNeoplasmsOxidative StressProtein Interaction MapsRenin-Angiotensin SystemAntineoplastic AgentsCYBA protein, humanMicroRNAsNADPH Oxidases

Identifiers

PMID33110473
PMCPMC7578723
OpenAlexW3095452189

What Socratic 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 Socratic graph.