Heart failure appears to be a severe public health problem affecting millions of people worldwide. Knowledge of the molecular mechanism contributing to ventricular remodeling would allow for earlier prevention of heart failure. Evidence exists reporting the involvement of IL-33 and ST2 and in heart remodeling. Thus, this study aims to delineate the effects of ST2 on chronic heart failure (CHF) via the IL-33/ST2 axis. Coronary artery ligation was employed to simulate CHF in rats, which were characterized by transthoracic echocardiography for cardiac function. After that, ST2 silencing and IL-33 overexpression were induced in rat models to evaluate apoptosis and pathological alterations in myocardial tissues and serum levels of biochemical indices. It was revealed that cardiac function was impaired in response to ST2 silencing. Furthermore, ST2 knockdown suppressed the activities of the mitochondrial respiratory chain and accelerated cardiomyocyte apoptosis via blockade of the IL-33/ST2 axis. These findings suggest an inhibitory role of ST2 silencing on the IL-33/ST2 axis, which consequently increases the risk of cardiac dysfunction, accelerates ventricular remodeling, and aggravates heart failure in rats. This study highlights that ST2 silencing may be a novel potential preventive or therapeutic target for CHF.
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http://dx.doi.org/10.1002/term.3091 | DOI Listing |
J Cell Mol Med
January 2025
NHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.
Proper differentiation of bone marrow stromal cells (BMSCs) into adipocytes is crucial for maintaining skeletal homeostasis. However, the underlying regulatory mechanisms remain incompletely understood, posing a challenge for the treatment of age-related osteopenia and osteoporosis. Here, through comprehensive gene expression analysis during BMSC differentiation into adipocytes, we identified the forkhead transcription factor Foxk2 as a key regulator of this process.
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January 2025
Department of Physiology, Nihon University School of Dentistry, 1-8-13, Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan.
Damage to the peripheral nerves of trigeminal ganglion (TG) neurons leads to intractable orofacial neuropathic pain through the induction of neuroinflammation. However, the details of this process are not yet fully understood. Here, we found that fibroblast-derived interleukin (IL)-33 was required for the development of mechanical allodynia in whisker pad skin following infraorbital nerve injury (IONI).
View Article and Find Full Text PDFOpen Life Sci
March 2024
Department of Breast Radiotherapy, Cancer Hospital Affiliated to Xinjiang Medical University, 789 Suzhou East Street, Xinshi District, Urumqi City, Xinjiang 830000, China.
Radiotherapy for treating breast cancer is associated with cardiac damage. This study aimed to investigate the role of the interleukin (IL)-33/soluble receptor ST2 (sST2) axis in radiation-induced cardiac injury. Expressions of IL-33 and sST2 were detected in breast cancer patients following radiotherapy, radiation-induced cardiac damaged mice model, and cardiomyocytes using quantitative real-time PCR (qRT-PCR) and immunohistochemical assay.
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January 2025
Department of Oncology, The First Affiliated Hospital of Henan University of CM, Zhengzhou, 450099, Henan, China.
Extranodal NK/T cell lymphoma (ENKTCL) is an extremely aggressive form of lymphoma and lacks of specific diagnostic markers. The study intended to unearth the role of interleukin-33 (IL-33) in ENKTCL. RT-qPCR was conducted to assess mRNA levels of ENKTCL tissues and cells, while western blot assay was performed for evaluating protein levels.
View Article and Find Full Text PDFFASEB J
December 2023
NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Adipogenesis is a tightly regulated process, and its dysfunction has been linked to metabolic disorders such as obesity. Forkhead box k1 (Foxk1) is known to play a role in the differentiation of myogenic precursor cells and tumorigenesis of different types of cancers; however, it is not clear whether and how it influences adipocyte differentiation. Here, we found that Foxk1 was induced in mouse primary bone marrow stromal cells (BMSCs) and established mesenchymal progenitor/stromal cell lines C3H/10T1/2 and ST2 after adipogenic treatment.
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