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Caspase-3/gasdermin-E axis facilitates the progression of coronary artery calcification by inducing the release of high mobility group box protein 1.
Yang, Honghui; Liu, Yingying; Chen, Gengyu; Zhou, Botong; Xu, Guian; Li, Qingman; Zhu, Lijie.
Afiliación
  • Yang H; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China. Electronic address: 19503809999@163.com.
  • Liu Y; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
  • Chen G; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
  • Zhou B; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
  • Xu G; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
  • Li Q; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
  • Zhu L; Department of Cardiology, Zhengzhou University, Central China Fuwai Hospital, Zhengzhou 451464, PR China.
Int Immunopharmacol ; 127: 111454, 2024 Jan 25.
Article en En | MEDLINE | ID: mdl-38159554
ABSTRACT
Coronary artery calcification (CAC) is commonly observed in atherosclerotic plaques, which is a pathogenic factor for severe coronary artery disease (CAD). The phenotype changes of vascular smooth muscle cells (VSMCs) are found to participate in CAC progression, which is mainly induced by vascular inflammation and oxidative stress (OS). HMGB1, a critical inflammatory cytokine, is recently reported to induce arterial calcification, which is regulated by the Caspase-3/gasdermin-E (GSDME) axis. However, the function of the Caspase-3/GSDME axis in CAC is unknown. Herein, the involvement of the Caspase-3/GSDME axis in CAC was studied to explore the possible targets for CAC. CAC model was constructed in mice, which was verified by red cytoplasm in coronary artery tissues, increased macrophage infiltration, aggravated inflammation, and enhanced RAGE signaling, accompanied by an increased release of HMGB1 and an activated Caspase-3/ GSDME axis. In ß-GP-treated MOVAS-1 cells, calcification, the ROS accumulation, enhanced LDH and HMGB1 release, enlarged macrophage production, aggravated inflammation, and activated RAGE signaling were observed, which were markedly abolished by the transfection of si-HMGB1 and si-GSDME. Moreover, the calcification deposition, the activity of Caspase-3/ GSDME axis, release of HMGB1, macrophage infiltration, cytokine production, and RAGE signaling in CAC mice were notably alleviated by VSMCs-specific GSDME knockdown, not by hematopoietic stem cells (HSCs)-specific GSDME knockdown. Collectively, Caspase-3/GSDME axis facilitated the progression of CAC by inducing the release of HMGB1.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de la Arteria Coronaria / Proteína HMGB1 Límite: Animals Idioma: En Revista: Int Immunopharmacol Asunto de la revista: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
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Imprimir
XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de la Arteria Coronaria / Proteína HMGB1 Límite: Animals Idioma: En Revista: Int Immunopharmacol Asunto de la revista: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos