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Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.
Acta Pharmacol Sin
January 2025
Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, State Key Laboratory of Cardiovascular Diseases, NHC Key Laboratory of Ischemic Heart Diseases, and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Pressure overload induces pathological cardiac remodeling, including cardiac hypertrophy and fibrosis, resulting in cardiac dysfunction or heart failure. Recently, we observed that the low-density lipoprotein receptor-related protein 6 (LRP6), has shown potential in enhancing cardiac function by mitigating cardiac fibrosis in a mouse model subjected to pressure overload. In this study, we investigated the role of LRP6 as a potential modulator of pressure overload-induced cardiac hypertrophy and elucidated the underlying molecular mechanisms.
View Article and Find Full Text PDF[Effect of overexpression of aldehyde dehydrogenase family member A2 on hypertrophic growth and proliferation of cardiomyocytes].
Sheng Wu Gong Cheng Xue Bao
December 2024
National Center for Protein Sciences (Beijing), Academy of Military Medical Sciences, Beijing 100850, China.
Retinoic acid signaling pathway plays a role in regulating vertebrate development, cell differentiation, and homeostasis. As a key enzyme that catalyzes the oxidation of retinal to retinoic acid, aldehyde dehydrogenase 1 family member A2 (Aldh1a2) is involved in cardiac development, while whether it functions in heart diseases remains to be studied. In this study, we infected primary cardiomyocytes with adenovirus overexpressing (Ad-Aldh1a2) to explore the effects of overexpression on the biological function of cardiomyocytes.
View Article and Find Full Text PDFSingle-cell RNA sequencing uncovers heterogenous immune cell responses upon exposure to food additive (E171) titanium dioxide.
J Nanobiotechnology
December 2024
Institute for Next Generation Material Design, Hanyang University, Seoul, 04763, Republic of Korea.
The prospective use of food additive titanium dioxide (E171 TiO) in a variety of fields (food, pharmaceutics, and cosmetics) prompts proper cellular cytotoxicity and transcriptomic assessment. Interestingly, smaller-sized E171 TiO can translocate in bloodstream and induce a diverse immunological response by activating the immune system, which can be either pro-inflammatory or immune-suppressive. Nevertheless, their cellular or immunologic responses in a heterogeneous population of the immune system following exposure of food additive E171 TiO is yet to be elucidated.
View Article and Find Full Text PDFOptimization of Potent and Selective Cyclohexyl Acid ERAP1 Inhibitors Using Structure- and Property-Based Drug Design.
ACS Med Chem Lett
December 2024
National Center for Scientific Research "Demokritos", Agia Paraskevi, Attiki 15341, Greece.
Endoplasmic reticulum aminopeptidase 1 (ERAP1) cleaves the -terminal amino acids of peptides, which can then bind onto major histocompatibility class I (MHC-I) molecules for presentation onto the cell surface, driving the activation of adaptive immune responses. In cancer, overtrimming of mature antigenic peptides can reduce cytotoxic T-cell responses, and ERAP1 can generate self-antigenic peptides which contribute to autoimmune cellular responses. Therefore, modulation of ERAP1 activity has potential therapeutic indications for cancer immunotherapy and in autoimmune disease.
View Article and Find Full Text PDFMast Cells Contribute to Pressure Overload-Induced Myocardial Hypertrophy by Upregulating TRPV4 via Histamine: Role of Ca2+/ CnA/NFATc3 Signaling Pathway.
Curr Med Sci
December 2024
Department of Cardiovasology, Affiliated Renhe Hospital of China Three Gorges University, Yichang, 443002, China.
Objective: To investigate whether cardiac mast cells (MCs) participate in pressure overload-induced myocardial hypertrophy through the regulation of transient receptor potential vanilloid 4 (TRPV4).
Methods: Pressure overload-induced myocardial hypertrophy was induced via abdominal aortic constriction (AAC). Myocardial hypertrophy was evaluated by measuring the heart weight index (HW/BW), lung weight index (LW/BW), ratio of heart weight to tibia length (HW/TL), ratio of lung weight to tibia length (LW/TL), and cross-sectional area of myocardial cells.
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