Cardiac remodelling is characterized by abnormal changes in the function and morphological properties such as diameter, mass, normal diameter of cavities, heart shape, fibrosis, thickening of vessels and heart layers, cardiomyopathy, infiltration of inflammatory cells, and some others. These damages are associated with damage to systolic and diastolic abnormalities, damage to ventricular function, and vascular remodelling, which may lead to heart failure and death. Exposure of the heart to radiation or anti-cancer drugs including chemotherapy drugs such as doxorubicin, receptor tyrosine kinase inhibitors (RTKIs) such as imatinib, and immune checkpoint inhibitors (ICIs) can induce several abnormal changes in the heart structure and function through the induction of inflammation and fibrosis, vascular remodelling, hypertrophy, and some others. This review aims to explain the basic mechanisms behind cardiac remodelling following cancer therapy by different anti-cancer modalities.
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http://dx.doi.org/10.1007/s12012-022-09762-6 | DOI Listing |
Adv Sci (Weinh)
December 2024
Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Aortic aneurysm is a life-threatening disease caused by progressive dilation of the aorta and weakened aortic walls. Its pathogenesis involves an imbalance between connective tissue repair and degradation. CD34 cells comprise a heterogeneous population that exhibits stem cell and progenitor cell properties.
View Article and Find Full Text PDFInflamm Regen
December 2024
Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) act together to regulate blood pressure and systemic blood flow by appropriately adjusting blood vessel diameter in response to biochemical or biomechanical stimuli. Ion channels that are expressed in these cells regulate membrane potential and cytosolic Ca concentration ([Ca]) in response to such stimuli. The subsets of these ion channels involved in Ca signaling often form molecular complexes with intracellular molecules via scaffolding proteins.
View Article and Find Full Text PDFSci Rep
December 2024
Clinical Department of Anesthesiology and Intensive Therapy, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
Coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB) is associated with the transient activation of a systemic inflammatory response. Fibronectin (FN), an endogenous inflammatory mediator, is a key component of the extracellular matrix. This study aimed to detect changes in cellular and plasma FN levels, as well as its potential fragmentation or FN-fibrin complex formation, in 40 patients undergoing CABG with CPB.
View Article and Find Full Text PDFVet Sci
November 2024
Department of Small Animal Clinical Science, School of Veterinary Science, University of Liverpool, Cardiology Service, Small Animal Teaching Hospital, Chester High Road, Neston CH64 7TE, UK.
The present study aimed to evaluate the effects of chronic pimobendan monotherapy on cardiac size in dogs with stage B2 myxomatous mitral valve disease (MMVD). Data from 31 dogs diagnosed with MMVD and cardiomegaly (LA/Ao ≥ 1.6 and LVIDdn ≥ 1.
View Article and Find Full Text PDFJ Cardiovasc Dev Dis
December 2024
Laboratory of X-Ray Endovascular and Reconstructive Cardiovascular Surgery, Department of Cardiovascular Surgery, Federal State Budgetary Institution "Research Institute for Complex Issues of Cardiovascular Diseases", Blvd. Named After Academician L.S. Barbarasha, 6, 650002 Kemerovo, Russia.
The Purpose: Evaluation of the short-term and long-term results of a phased correction of the tetralogy of Fallot (ToF) with stenting of the right ventricular outflow tract (RVOT) in comparison with a one-stage total correction (TC) of the defect.
Materials And Methods: Two groups of patients with classical ToF were formed. Group 1 (n = 25; median age = 72 days) was initially represented by children with ToF with a more severe clinical status (median weight = 3.
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