Prokineticin Receptor-1 Signaling Inhibits Dose- and Time-Dependent Anthracycline-Induced Cardiovascular Toxicity Via Myocardial and Vascular Protection

Gasser, Adeline; Chen, Yu‐Wen; Audebrand, Anais; Daglayan, Ayhan; Charavin, Marine; Escoubet, Brigitte; Karpov, P F; Tetko, Igor V.; Chan, Michael W.Y.; Cardinale, Daniela; Désaubry, Laurent; Nebigil, Canan G.

doi:10.1016/j.jaccao.2019.06.003

Cited by 11 publications

(21 citation statements)

References 39 publications

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“…A recent study identified the molecular and cellular signature of dose-dependent, doxorubicin-mediated cardiotoxicity and provided evidence that prokineticin receptor (PKR-1)-1, acting at myocardial and vascular level, is a promising target to combat cardiotoxicity of cancer treatments (104).…”

Section: Perspectivesmentioning

confidence: 99%

Cardiotoxicity of Anthracyclines

Cardinale

Fabiani

Cipolla

2020

Front. Cardiovasc. Med.

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235

162

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Cardiotoxicity is a feared side effect that may limit the clinical use of anthracyclines. It may indeed affect the quality of life and survival of patients with cancer, regardless of oncological prognosis. This paper provides an overview of anthracycline-induced cardiotoxicity in terms of definition, classification, incidence, risk factors, possible mechanisms, diagnosis, and treatment. We also report effective strategies for preventing cardiotoxicity. In addition, we discuss limiting current approaches, the need for a new classification, and early cardiotoxicity detection and treatment. Probably, anthracycline-induced cardiotoxicity is a continuous phenomenon that starts from myocardial cell injury; it is followed by left ventricular ejection fraction (LVEF) and, if not diagnosed and cured early, progressively leads to symptomatic heart failure. Anthracycline-induced cardiotoxicity can be detected at a preclinical phase. The role of biomarkers, in particular troponins, in identifying subclinical cardiotoxicity and its therapy with angiotensin-converting enzyme inhibitors (mainly enalapril) to prevent LVEF reduction is a recognized and effective strategy. If cardiac dysfunction has already occurred, partial or complete LVEF recovery may still be obtained in case of early detection of cardiotoxicity and prompt heart failure treatment.

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Section: Perspectivesmentioning

confidence: 99%

Cardiotoxicity of Anthracyclines

Cardinale

Fabiani

Cipolla

2020

Front. Cardiovasc. Med.

Self Cite

235

162

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“…These receptors have also divergent effects on ECs ( 101 ). Thus, a non-peptide agonist specific for PKR1, called IS20, was developed to mimic the cardioprotective effects of PROK2 against heart failure developed by myocardial infarction ( 102 ) and anthracyclines ( 6 ) in mice.…”

Section: New Horizons In Therapeutic Strategies: Pro-angiogenic Therapy To Prevent Vascular Toxicity Without Altering Anti-neoplastic Promentioning

confidence: 99%

“…Vascular damage in the cardiovascular system can be caused not only by anti-angiogenic chemotherapy (inhibitors of vascular endothelial growth factor (VEGFi), but also by anti-tumor antibiotics (bleomycin and anthracyclines) ( 5 , 6 ). The first line of treatments includes monoclonal antibodies (e.g., bevacizumab), and multiple kinase inhibitors such as sunitinib, a multi-targeted inhibitor, or sorafenib ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

“…Reduced concentration of NO shifts endothelium to a pro-coagulant status and impairs vasodilatation ( 33 ). Recently, doxorubicin has been shown to stabilize NRF2 in the cytoplasm thereby reducing detoxification pathway in mice heart ( 6 ). Doxorubicin also induces mitochondrial DNA damage in an RNS/ROS-independent manner, along with a possible decrease in B-cell lymphoma (Bcl)-2, that leads to apoptosis of the ECs.…”

Section: Introductionmentioning

confidence: 99%

“…A recent preclinical study has shown that chronic treatment with doxorubicin promotes vessel rarefaction in the heart ( 6 ). Moreover, a low dose of doxorubicin inhibits EC motility in vitro without causing apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Updates on Anticancer Therapy-Mediated Vascular Toxicity and New Horizons in Therapeutic Strategies

Hsu

Mammadova

Benkirane‐Jessel

et al. 2021

Front. Cardiovasc. Med.

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Vascular toxicity is a frequent adverse effect of current anticancer chemotherapies and often results from endothelial dysfunction. Vascular endothelial growth factor inhibitors (VEGFi), anthracyclines, plant alkaloids, alkylating agents, antimetabolites, and radiation therapy evoke vascular toxicity. These anticancer treatments not only affect tumor vascularization in a beneficial manner, they also damage ECs in the heart. Cardiac ECs have a vital role in cardiovascular functions including hemostasis, inflammatory and coagulation responses, vasculogenesis, and angiogenesis. EC damage can be resulted from capturing angiogenic factors, inhibiting EC proliferation, survival and signal transduction, or altering vascular tone. EC dysfunction accounts for the pathogenesis of myocardial infarction, atherothrombosis, microangiopathies, and hypertension. In this review, we provide a comprehensive overview of the effects of chemotherapeutic agents on vascular toxicity leading to hypertension, microvascular rarefaction thrombosis and atherosclerosis, and affecting drug delivery. We also describe the potential therapeutic approaches such as vascular endothelial growth factor (VEGF)-B and prokineticin receptor-1 agonists to maintain endothelial function during or following treatments with chemotherapeutic agents, without affecting anti-tumor effectiveness.

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Prokineticin signaling in heart-brain developmental axis: Therapeutic options for heart and brain injuries

Désaubry

Kanthasamy

Nebigil

2020

Pharmacological Research

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Heart and brain development occur simultaneously during the embryogenesis, and both organ development and injuries are interconnected. Early neuronal and cardiac injury share mutual cellular events, such as angiogenesis and plasticity that could either delay disease progression or, in the long run, result in detrimental health effects. For this reason, the common mechanisms provide a new and previously undervalued window of opportunity for intervention.Because angiogenesis, cardiogenesis and neurogenesis are essential for the development and regeneration of the heart and brain, we discuss therein the role of prokineticin as an angiogenic neuropeptide in heart-brain development and injuries. We focus on the role of prokineticin signaling and the effect of drugs targeting prokineticin receptors in neuroprotection and cardioprotection, with a special emphasis on heart failure, neurodegenerative Parkinson's disease and ischemic heart and brain injuries. Indeed, prokineticin triggers common pro-survival signaling pathway in heart and brain.Our review aims at stimulating researchers and clinicians in neurocardiology to focus on the role of prokineticin signaling in the reciprocal interaction between heart and brain. We hope to facilitate the discovery of new treatment strategies, acting in both heart and brain degenerative diseases.

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Prokineticin Receptor-1 Signaling Inhibits Dose- and Time-Dependent Anthracycline-Induced Cardiovascular Toxicity Via Myocardial and Vascular Protection

Cited by 11 publications

References 39 publications

Cardiotoxicity of Anthracyclines

Cardiotoxicity of Anthracyclines

Updates on Anticancer Therapy-Mediated Vascular Toxicity and New Horizons in Therapeutic Strategies

Prokineticin signaling in heart-brain developmental axis: Therapeutic options for heart and brain injuries

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