Macrophage NLRP3 inflammasome mediates the effects of sympathetic nerve on cardiac remodeling in obese rats DOI Creative Commons
Zhaoqing Xi, Ling Shu,

Lingling Xiao

и другие.

Molecular and Cellular Endocrinology, Год журнала: 2024, Номер 596, С. 112417 - 112417

Опубликована: Ноя. 16, 2024

Obesity-associated cardiac remodeling is characterized by sympathetic nerve over-activation and pro-inflammatory macrophage infiltration. We identified norepinephrine (NE), a neurotransmitter, as effector to activate NLRP3 inflammasome, which contributed inflammation. In vivo, Sprague-Dawley (SD) rats were fed high-fat diet (HFD) for 12 weeks establish obese rat models. Obese exhibited marked hypertrophy compared normal rats. The expression of interleukin (IL)-1β was upregulated, accompanied CD68+NLRP3+ infiltration in the hearts also showed increased activity. β-adrenergic receptor (AR) inhibition mitigated these changes. vitro, neurotransmitter NE significantly exacerbated palmitic acid (PA)-induced polarization toward type inflammasome activation THP-1 macrophages. It further found that role dependent on protein kinase A (PKA) subsequently β-arrestin2, an important regulator nuclear factor-kappa B (NF-κB) pathway. This study identifies neuro-immune axis mediator obesity-associated remodeling. Targeting system may open therapeutic opportunities treatment obesity.

Язык: Английский

Exercise-induced adipokine Nrg4 alleviates MASLD by disrupting hepatic cGAS-STING signaling DOI Creative Commons
Min Chen, Yang Li,

Jieying Zhu

и другие.

Cell Reports, Год журнала: 2025, Номер 44(2), С. 115251 - 115251

Опубликована: Янв. 31, 2025

Язык: Английский

Процитировано

2

Role of deubiquitinase USP47 in cardiac function alleviation and anti-inflammatory immunity after myocardial infarction by regulating NLRP3 inflammasome-mediated pyroptotic signal pathways DOI

Zheng Wu,

Wenzheng Li,

Shaoping Wang

и другие.

International Immunopharmacology, Год журнала: 2024, Номер 136, С. 112346 - 112346

Опубликована: Июнь 7, 2024

Язык: Английский

Процитировано

4

BAM15 Inhibits Endothelial Pyroptosis via the NLRP3/ASC/caspase-1 Pathway to Alleviate Atherosclerosis DOI

Su Zhong,

Hui Shen, Xiaoman Dai

и другие.

Atherosclerosis, Год журнала: 2025, Номер 406, С. 119226 - 119226

Опубликована: Май 1, 2025

Язык: Английский

Процитировано

0

Aerobic Exercise and PI3K Inhibitor Ameliorate Obesity Cardiomyopathy by Alleviating Pyroptosis in Middle-Aged Mice DOI Open Access
Bin Yang, Jiahao Xu,

Xiaofang Dao

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(10), С. 4935 - 4935

Опубликована: Май 21, 2025

Obesity cardiomyopathy (OCM) represents a rapidly growing health concern globally, characterized by metabolic, structural, and functional abnormalities of the heart. Current research has demonstrated that inflammation plays pivotal role in obesity-induced cardiomyopathy, regular exercise can ameliorate lipid disturbances inflammatory effectively. However, underlying mechanisms are not fully elucidated. We investigated effects an 8-week aerobic intervention on myocardial structure, function, HFD-induced obese mice. The results revealed alleviated myocardium pyroptosis down-regulating PI3K/AKT signaling pathway. Furthermore, inhibition PI3K pathway LY294002, coupled with exercise, attenuated suppressed impairments, inflammation, pyroptosis, synergistic effect. Based these findings, we concluded eight weeks synergizes through to improve obesity-associated remodeling dysfunction. Therefore, long-term potential strategy treatment OCM.

Язык: Английский

Процитировано

0

Macrophage NLRP3 inflammasome mediates the effects of sympathetic nerve on cardiac remodeling in obese rats DOI Creative Commons
Zhaoqing Xi, Ling Shu,

Lingling Xiao

и другие.

Molecular and Cellular Endocrinology, Год журнала: 2024, Номер 596, С. 112417 - 112417

Опубликована: Ноя. 16, 2024

Obesity-associated cardiac remodeling is characterized by sympathetic nerve over-activation and pro-inflammatory macrophage infiltration. We identified norepinephrine (NE), a neurotransmitter, as effector to activate NLRP3 inflammasome, which contributed inflammation. In vivo, Sprague-Dawley (SD) rats were fed high-fat diet (HFD) for 12 weeks establish obese rat models. Obese exhibited marked hypertrophy compared normal rats. The expression of interleukin (IL)-1β was upregulated, accompanied CD68+NLRP3+ infiltration in the hearts also showed increased activity. β-adrenergic receptor (AR) inhibition mitigated these changes. vitro, neurotransmitter NE significantly exacerbated palmitic acid (PA)-induced polarization toward type inflammasome activation THP-1 macrophages. It further found that role dependent on protein kinase A (PKA) subsequently β-arrestin2, an important regulator nuclear factor-kappa B (NF-κB) pathway. This study identifies neuro-immune axis mediator obesity-associated remodeling. Targeting system may open therapeutic opportunities treatment obesity.

Язык: Английский

Процитировано

0