iBet uBet web content aggregator. Adding the entire web to your favor.
iBet uBet web content aggregator. Adding the entire web to your favor.



Link to original content: https://pubmed.ncbi.nlm.nih.gov/28911261
Out of the frying pan and into the fire: damage-associated molecular patterns and cardiovascular toxicity following cancer therapy - PubMed Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Nov;11(11):297-317.
doi: 10.1177/1753944717729141. Epub 2017 Sep 15.

Out of the frying pan and into the fire: damage-associated molecular patterns and cardiovascular toxicity following cancer therapy

Nicole S Klee  1 , Cameron G McCarthy  2 , Patricia Martinez-Quinones  3 , R Clinton Webb  2
Affiliations
Review

Out of the frying pan and into the fire: damage-associated molecular patterns and cardiovascular toxicity following cancer therapy

Nicole S Klee et al. Ther Adv Cardiovasc Dis. 2017 Nov.

Abstract

Cardio-oncology is a new and rapidly expanding field that merges cancer and cardiovascular disease. Cardiovascular disease is an omnipresent side effect of cancer therapy; in fact, it is the second leading cause of death in cancer survivors after recurrent cancer. It has been well documented that many cancer chemotherapeutic agents cause cardiovascular toxicity. Nonetheless, the underlying cause of cancer therapy-induced cardiovascular toxicity is largely unknown. In this review, we discuss the potential role of damage-associated molecular patterns (DAMPs) as an underlying contributor to cancer therapy-induced cardiovascular toxicity. With an increasing number of cancer patients, as well as extended life expectancy, understanding the mechanisms underlying cancer therapy-induced cardiovascular disease is of the utmost importance to ensure that cancer is the only disease burden that cancer survivors have to endure.

Keywords: cancer therapy; cardio-oncology; cardiotoxicity; cardiovascular disease; damage-associated molecular patterns; inflammation.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest statement: The authors declare that there is no conflict of interest.

Figures

Figure 1.
Figure 1.
Common risk factors that contribute to both cancer and cardiovascular disease. Adapted from Irvine Page’s Mosaic Theory of Hypertension.
Figure 2.
Figure 2.
Hypothesized schematic of how damage-associated molecular patterns (DAMPs) contribute to the treatment and progression of cancer and cardiotoxicity. Due to the paradoxical contribution of DAMPs to cancer progression in the literature, we believe two key thresholds of DAMP expression exist. The first is the ‘anti-cancer’ threshold and this is where controlled amounts of DAMPs stimulate the immune system to mount an effective defense against the growing and potentially pathogenic tumor. This explains the benefits of immunogenic cell death (ICD) to cancer remission. The second threshold is the one of pathogenicity and this is when DAMP expression becomes so excessive and chronic that uncontrolled inflammation ensues, and this contributes to the progression of cancer, resistance to anti-cancer treatments, and cardiovascular disease. DAMPs, damage-associated molecular patterns.
Figure 3.
Figure 3.
Danger signaling in cardio-oncology. The nature of cancer therapy is to reduce tumor size by causing sudden and rapid cancer-cell death. Because damage-associated molecular patterns (DAMPs) are released from dead and dying cells (via necrosis or apoptosis), this results in the release of DAMPs from cells during cancer therapy. DAMPs activate the immune system through activation of pattern-recognition receptors from cell types within the cardiovascular system (e.g. endothelial cells, vascular smooth muscle); we hypothesize that the overactivation of this system results in a pro-inflammatory cardiovascular disease following cancer therapy. DAMPs, damage-associated molecular patterns.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. American Cancer Society. Cancer treatment and survivorship: facts and figures 2016-2017. Atlanta 2016, https://www.cancer.gov/publications/dictionaries/cancer-terms?CdrID=44004.
    1. Wickramasinghe CD, Nguyen KL, Watson KE, et al. Concepts in cardio-oncology: definitions, mechanisms, diagnosis and treatment strategies of cancer therapy-induced cardiotoxicity. Future Oncol 2016; 12: 855–870. - PubMed
    1. Okwuosa TM, Anzevino S, Rao R. Cardiovascular disease in cancer survivors. Postgrad Med J 2017; 93: 82–90. - PubMed
    1. Landy DC, Miller TL, Lopez-Mitnik G, et al. Aggregating traditional cardiovascular disease risk factors to assess the cardiometabolic health of childhood cancer survivors: an analysis from the Cardiac Risk Factors in Childhood Cancer Survivors Study. Am Heart J 2012; 163: 295–301.e2. - PMC - PubMed
    1. Mulrooney DA, Armstrong GT, Huang S, et al. Cardiac outcomes in adult survivors of childhood cancer exposed to cardiotoxic therapy: a cross-sectional study. Ann Intern Med 2016; 164: 93–101. - PMC - PubMed

MeSH terms

LinkOut - more resources