Cited by 915Chemotherapy-induced cardiotoxicity and mitigationCardiomyopathy and Myosin StudiesCardiovascular Function and Risk Factors

The DOI matches its Crossref record; 192 of the 198 references it cites were found in a registry or an index.

Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management

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Abstract

homeostasis, autophagy, the release of nitric oxide and inflammatory mediators and altered gene and protein expression that involved apoptosis. Dox also causes downregulation of DNA methyltransferase 1 (DNMT1) enzyme activity which leads to a reduction in the DNA methylation process. This hypomethylation causes dysregulation in the mitochondrial genes like peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1-alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM) unit in the heart. Apart from DNA methylation, Dox treatment also alters the micro RNAs levels and histone deacetylase (HDAC) activity. Therefore, in the current review, we have provided a detailed update on the current understanding of the pathological mechanisms behind the well-known Dox-induced cardiotoxicity. Further, we have provided some of the most plausible pharmacological strategies which have been tested against Dox-induced cardiotoxicity.

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Crossref · 10.1016/j.biopha.2021.111708

Cites

192 of 192 references verified0 citation errors · 0 not checkable

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Citations

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2 retracted

Show all 198 references

Research works printed but not linked: 6

  1. Gianni, 2008, Anthracycline cardiotoxicity: from bench to bedside, J. Clin. Oncol.: Off. J. Am. Soc. Clin. Oncol., 26, 3777, 10.1200/JCO.2007.14.9401 · DOI
  2. Chustecka, 2006, Cardiotoxicity of imatinib is a" surprise, Nat. Med., 24
  3. Martínez-Mateo, 2017, Report of cisplatin-induced cardiotoxicity: a side effect to monitor closely, J. Heart Health, 3
  4. Speth, 1988, Clinical pharmacokinetics of doxorubicin, Clin. Pharmacokinet., 15, 15, 10.2165/00003088-198815010-00002 · DOI
  5. Youngson, 2006, Collins dictionary of human biology, Collins
  6. Zhu, 2009, Acute doxorubicin cardiotoxicity is associated with p53-induced inhibition of the mTOR pathway, Circulation, 119, 99, 10.1161/CIRCULATIONAHA.108.799700 · DOI

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Metadata

Authors
Rawat, P. S., Jaiswal, A., Khurana, A., Bhatti, J. S., & Navik, U.
Affiliations
  • Central University of Punjab (IN)
  • P.V. Narsimha Rao Telangana Veterinary University (IN)
Venue
Biomedicine & Pharmacotherapy
Publisher
Elsevier BV
Published
2021-07
Volume
139
Pages
111708
ISSN
0753-3322 (ISSN-L)
OpenAlex
W3160992829
Cited by
909
References
198
Citations by year
2026: 171 · 2025: 232 · 2024: 208 · 2023: 193 · 2022: 92 · 2021: 13
FWCI
24.68
Type
journal article
Language
en
Open access
Locations
  • Biomedicine & Pharmacotherapy (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Royal Society of Medicine
  • University of Central Punjab (GP-25)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Chemotherapy-induced cardiotoxicity and mitigation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
doxorubicin, cardiotoxicity, molecular mechanisms, DNA methylation, DNMT1, mitochondrial dysfunction, PGC-1α, NRF1, TFAM, microRNA, histone deacetylase, autophagy, apoptosis, nitric oxide, inflammatory mediators, cardioprotection, anthracycline chemotherapy
MeSH terms
Animals, Antibiotics, Antineoplastic, Doxorubicin, Humans, Mitochondria, Heart, Apoptosis, Oxidative Stress, Cardiotoxicity

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