Radiation therapy is one of the most important methods for the treatment of malignant tumors. However, in radiotherapy for thoracic tumors such as breast cancer, lung cancer, esophageal cancer, and mediastinal lymphoma, the heart, located in the mediastinum, is inevitably affected by the irradiation, leading to pericardial disease, myocardial fibrosis, coronary artery disease, valvular lesions, and cardiac conduction system injury, which are considered radiation-induced heart diseases. Delayed cardiac injury especially myocardial fibrosis is more prominent, and its incidence is as high as 20–80%. Myocardial fibrosis is the final stage of radiation-induced heart diseases, and it increases the stiffness of the myocardium and decreases myocardial systolic and diastolic function, resulting in myocardial electrical physiological disorder, arrhythmia, incomplete heart function, or even sudden death. This article reviews the pathogenesis and prevention of radiation-induced myocardial fibrosis for providing references for the prevention and treatment of radiation-induced myocardial fibrosis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464468 | PMC |
http://dx.doi.org/10.22034/APJCP.2017.18.3.583 | DOI Listing |
Arrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5000 people globally and is caused by mutations in cardiac desmosomal proteins including , and Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals. Here we performed single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics on myocardial samples from patients with ACM and control donors.
View Article and Find Full Text PDFClin Transl Med
January 2025
Key Laboratory For Organ Failure Research, Ministry of Education of the People's Republic of China, Guangzhou, China.
Introduction: Heart failure with preserved ejection fraction (HFpEF) is a complex condition characterized by metabolic dysfunction and myocardial lipotoxicity. The roles of PTEN-induced kinase 1 (PINK1) and peroxiredoxin-2 (Prdx2) in HFpEF pathogenesis remain unclear.
Objective: This study aimed to investigate the interaction between PINK1 and Prdx2 to mitigate cardiac diastolic dysfunction in HFpEF.
J Transl Med
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Background: Dilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Infiltration and alterations in non-cardiomyocytes of the human heart involve crucially in the occurrence of DCM and associated immunotherapeutic approaches.
Methods: We constructed a single-cell transcriptional atlas of DCM and normal patients.
Zhonghua Bing Li Xue Za Zhi
January 2025
Department of Pathology, the Seventh Medical Center of People's Liberation Army of China General Hospital, Beijing100700, China.
To analyze the morphologic changes and the extent of severity in end-stage heart disease; and to explore the correlation with their clinical features. Twelve cases of recipients who underwent pediatric cardiac allograft transplantation were collected from May 2022 to November 2023 at the Seventh Medical Center of People's Liberation Army of China General Hospital. Gross pathologic examinations were performed and morphological changes were observed under a light microscope after HE, Masson's trichrome, and reticulin staining.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
Department of Cardiac Surgery, Peking University Third Hospital, Beijing 100191, China. Electronic address:
Chronic heart failure, caused by myocardial fibrosis after acute myocardial infarction (AMI), remains a serious clinical problem that needs urgent resolution. Nitro-oleic acid (OA-NO), an electrophilic nitro-fatty acid found in human plasma, is believed to regulate various pathophysiological functions, particularly anti-inflammation and anti-fibrosis. However, the role of OA-NO in AMI remains unexplored.
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