scholarly journals Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics

2021 ◽  
Vol 14 (10) ◽  
pp. 970
Author(s):  
Archana Adhikari ◽  
Syed Mohammed Basheeruddin Asdaq ◽  
Maitham A. Al Hawaj ◽  
Manodeep Chakraborty ◽  
Gayatri Thapa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Anticancer Drug ◽  
Protective Role ◽  
Dramatic Improvement ◽  
Future Perspectives ◽  
Drug Induced ◽  
Chemotherapy Drugs ◽  
Life Threatening ◽  
Rate Of Recovery

The advancement in therapy has provided a dramatic improvement in the rate of recovery among cancer patients. However, this improved survival is also associated with enhanced risks for cardiovascular manifestations, including hypertension, arrhythmias, and heart failure. The cardiotoxicity induced by chemotherapy is a life-threatening consequence that restricts the use of several chemotherapy drugs in clinical practice. This article addresses the prevalence of cardiotoxicity mediated by commonly used chemotherapeutic and immunotherapeutic agents. The role of susceptible genes and radiation therapy in the occurrence of cardiotoxicity is also reviewed. This review also emphasizes the protective role of antioxidants and future perspectives in anticancer drug-induced cardiotoxicities.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

scholarly journals Therapeutic Role of Tocilizumab in SARS-CoV-2-Induced Cytokine Storm: Rationale and Current Evidence

2021 ◽  
Vol 22 (6) ◽  
pp. 3059
Author(s):  
Corrado Pelaia ◽  
Cecilia Calabrese ◽  
Eugenio Garofalo ◽  
Andrea Bruni ◽  
Alessandro Vatrella ◽  
...  
Keyword(s):  
Review Article ◽  
Lung Damage ◽  
Current Evidence ◽  
Therapeutic Effects ◽  
Cytokine Storm ◽  
Future Perspectives ◽  
Pathogenic Role ◽  
Refractory Rheumatoid Arthritis ◽  
Life Threatening

Among patients suffering from coronavirus disease 2019 (COVID-19) syndrome, one of the worst possible scenarios is represented by the critical lung damage caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)-induced cytokine storm, responsible for a potentially very dangerous hyperinflammatory condition. Within such a context, interleukin-6 (IL-6) plays a key pathogenic role, thus being a suitable therapeutic target. Indeed, the IL-6-receptor antagonist tocilizumab, already approved for treatment of refractory rheumatoid arthritis, is often used to treat patients with severe COVID-19 symptoms and lung involvement. Therefore, the aim of this review article is to focus on the rationale of tocilizumab utilization in the SARS-CoV-2-triggered cytokine storm, as well as to discuss current evidence and future perspectives, especially with regard to ongoing trials referring to the evaluation of tocilizumab’s therapeutic effects in patients with life-threatening SARS-CoV-2 infection.

Abstract 507: Activation of the Classically Pro-Apoptotic Death Receptor 5 Promotes Physiological Hypertrophy and Cardiomyocyte Survival

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Toby Thomas ◽  
Miles Tanner ◽  
Laurel Grisanti
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Fibrosis ◽  
Death Receptor ◽  
Protective Role ◽  
Cardiomyocyte Hypertrophy ◽  
Death Receptor 5 ◽  
Tnf Α ◽  
Cardiomyocyte Survival

Heart failure is hallmarked by a combination of cardiomyocyte hypertrophy and death. Apoptosis, one of the primary mechanisms of cell death, occurs through finely tuned extrinsic or intrinsic pathways. Of the mediators involved in extrinsic apoptotic signaling, some have been extensively studied, such as tumor necrosis factor ((TNF)-α), while others have been relatively untouched. One such receptor is Death Receptor 5 (DR5) which, along with its ligand TNF-Related Apoptosis Inducing Ligand (TRAIL), have recently been implicated as a biomarker in determining the progression and outcome in patients following multiple heart failure etiologies, suggesting a novel role of DR5 signaling in the heart. These studies suggest a potentially protective role for DR5 in the heart; however, the function of TRAIL/DR5 in the heart has been virtually unstudied. Our goal was to explore the role of TRAIL/DR5 in cardiomyocyte hypertrophy and survival with the hypothesis that DR5 promotes cardiomyocyte survival and growth through non-canonical mechanisms. Mice treated with the DR5 agonist bioymifi or a DR5 agonist antibody, MD5-1, were absent of cell death, while an increase in hypertrophy was observed without a decline in cardiac function. In isolated cardiomyocytes, this pro-hypertrophic phenotype was determined to operate through MMP-dependent cleavage of HB-EGFR, leading to transactivation of EGFR and ERK1/2 signaling. To determine the role of DR5 in heart failure, a chronic catecholamine administration model was used and DR5 activation was found to decrease cardiomyocyte death and cardiac fibrosis. ERK1/2, a well characterized pro-survival, pro-hypertrophic kinase is activated in the heart with DR5 agonist administration and may represent the mechanistic link through which DR5 is imparting cardioprotection. In summary, DR5 activation promotes cardiomyocyte hypertrophy and survival and prevents cardiac fibrosis via a non-canonical MMP-EGFR-ERK1/2 pathway. Taken together, these studies identify a previously undetermined role for DR5 in the heart and identify novel therapeutic target for the treatment of heart failure.

Mo1031 PROTECTIVE ROLE OF THE PRO-RESOLVING LIPID MEDIATOR RESOLVIN D1 IN NONSTEROIDAL ANTI-INFLAMMATORY DRUG-INDUCED SMALL INTESTINAL DAMAGE

2020 ◽  
Vol 158 (6) ◽  
pp. S-762
Author(s):  
Takuya Kuzumoto ◽  
Tetsuya Tanigawa ◽  
Hiroyuki Kitamura ◽  
Akira Higashimori ◽  
Yuji Nadatani ◽  
...  
Keyword(s):  
Protective Role ◽  
Lipid Mediator ◽  
Intestinal Damage ◽  
Resolvin D1 ◽  
Drug Induced ◽  
Inflammatory Drug ◽  
Small Intestinal ◽  
Anti Inflammatory

The role of nutrition in critical care

2020 ◽  
Vol 11 (4) ◽  
pp. 166-171
Author(s):  
Kathryn Latimer-Jones
Keyword(s):  
Critically Ill ◽  
Critically Ill Patients ◽  
Physiological Stress ◽  
Active Role ◽  
Drug Induced ◽  
Increased Risk ◽  
Anorexic Patient ◽  
Life Threatening ◽  
Improve Patient

Critically ill patients have conditions that are considered life-threatening and require comprehensive care and constant monitoring; nutritional support plays a key role in the recovery of these patients and is an area of veterinary medicine that is very easy for the registered veterinary nurse (RVN) to have an active role in. Critically ill patients are at increased risk of malnutrition; acute and chronic illness, trauma and inflammation induced stress-related catabolism, and drug-induced adverse effects may reduce appetite or increase nausea and vomiting. Challenges exist in the provision of support, especially in the anorexic patient. This article focuses on how severe physiological stress affects animals that are critically ill and how this might lead to malnutrition, how to accurately calculate energy requirements, and discusses the importance of selecting the most appropriate diet to improve patient outcomes.

scholarly journals Congestive heart failure induces endothelial cell apoptosis: protective role of carvedilol

2000 ◽  
Vol 36 (7) ◽  
pp. 2081-2089 ◽  
Author(s):  
Lothar Rössig ◽  
Judith Haendeler ◽  
Ziad Mallat ◽  
Benedicte Hugel ◽  
Jean-Marie Freyssinet ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Protective Role ◽  
Endothelial Cell Apoptosis

Protective Role of Medications on Atrial Fibrillation and Heart Failure with Preserved Ejection Fraction

2014 ◽  
Vol 20 (8) ◽  
pp. S121
Author(s):  
Arnav Kumar ◽  
Amarpreet K. Saluja ◽  
Adnan Khan ◽  
Mohammad Morsy ◽  
Wissam I. Khalife
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Ejection Fraction ◽  
Protective Role ◽  
Preserved Ejection Fraction

scholarly journals Protective Effect of Quercetin on Melphalan-Induced Oxidative Stress and Impaired Renal and Hepatic Functions in Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ebenezer Tunde Olayinka ◽  
Ayokanmi Ore ◽  
Olaniyi Solomon Ola ◽  
Oluwatobi Adewumi Adeyemo
Keyword(s):  
Anticancer Agents ◽  
Hepatic Function ◽  
Protective Role ◽  
Glutathione S Transferase ◽  
Drug Induced ◽  
Treatment Groups ◽  
Plasma Bilirubin ◽  
Male Wistar Rats ◽  
Mda Content

One major challenge with the use of anticancer agents is the phenomenon of drug-induced toxicity. Melphalan (MPLN) is an alkylating anticancer agent, while quercetin (QCT) is an antioxidant. We investigated the protective role of quercetin against MPLN-induced toxicity. Twenty-five male Wistar rats (160–170 g) were randomized into five treatment groups; (I) control, (II) MPLN (0.2 mg/kg b.w.), (III) pre-treated with QCT (20 mg/kg b.w.) for 7 days followed by MPLN (0.2 mg/kg b.w.) for 7 days, (IV) cotreated with QCT (20 mg/kg b.w.) and MPLN (0.2 mg/kg b.w.) for 7 days, and (V) QCT (20 mg/kg b.w.) alone. MPLN caused a significant increase in plasma bilirubin, urea, and creatinine by 122.2%, 102.3%, and 188%, respectively (P<0.05). Similarly, plasma ALP, ALT, AST, and γ-GT activities increased significantly by 57.9%, 144.3%, 71.3%, and 307.2%, respectively, relative to control. However, pre or cotreatment with QCT ameliorated the levels of renal and hepatic function indices. Hepatic ascorbic acid and GSH and activities of glutathione-S-transferase, SOD, and catalase decreased significantly by 36.2%, 188%, 46.5%, 34.4%, and 55.2%, respectively, followed by increase in MDA content by 46.5% relative to control. Pre- and cotreatment with QCT reestablished the hepatic antioxidant status and lipid peroxidation. Overall, quercetin protected against MPLN-induced renal and hepatic toxicity in rats.

scholarly journals (Letter to the Editor) Response to: protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 73-74
Author(s):  
Natalia López-Andrés
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Cardiac Fibroblasts ◽  
Direct Consequence ◽  
Protective Role ◽  
Mitochondrial Proteins ◽  
Galectin 3 ◽  
Human Cardiac Fibroblasts

Abstract We thank Ahmed et al. for their letter regarding our study ‘Galectin-3 down-regulates antioxidant peroxiredoxin-4 in human cardiac fibroblasts’ [1]. As emphasized by Ahmed et al., Prx-4 levels decrease [2] whereas MFN-2, OPA-1 and PGC-1α levels increase [3] in dilated cardiomyopathy (DCM). Moreover, Gal-3 expression is also increased in DCM [4]. In our study, we showed in vitro that Gal-3 decreased Prx-4 without modifying MFN-2 or PGC-1α levels in human cardiac fibroblasts. Although cardiac Prx-4 decrease could be a direct consequence of Gal-3 effects on cardiac fibroblasts, we cannot exclude the possibility that other factors increase MFN-2, OPA-1 and PGC-1α levels in both cardiac fibroblasts or cardiomyocytes in the context of DCM. Further studies are needed to clarify the association between Prx-4 decrease and the increase in other mitochondrial proteins in DCM.

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