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Periodontitis is a chronic inflammatory condition mainly caused by the interaction between the host immune system and periodontal tissue pathogens, and may lead to consequences, such as alveolar bone defects and tooth loss. Incomplete bacterial removal, persistent inflammation and high reactive oxygen species (ROS) environment are the main challenges for periodontal tissue repair and alveolar bone regeneration. In this study, an injectable composite microgel (Gelatin methacryloyl-Phenylboronic acid/Hydroxyadamantane, GPH) loaded with antimicrobial peptide (AMP) and cerium dioxide (CeO) microspheres was developed to achieve a synergistic function of bacteriostasis, immunomodulation, and ROS removal.

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RGFP966 inhibits palmitic acid induced VSMCs phenotypic transition by targeting ATGL.

Biochim Biophys Acta Mol Cell Biol Lipids

January 2025

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address:

Background: The phenotypic switch of vascular smooth muscle cells (VSMCs) underlies the pathology of many cardiovascular diseases. Histone deacetylase 3 (HDAC3) is reported to upregulate in several cardiovascular diseases. RGFP966 is a highly selective HDAC3 inhibitor.

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Glycocalyx disruption, endothelial dysfunction and vascular remodeling as underlying mechanisms and treatment targets of chronic venous disease.

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Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA -

The glycocalyx is an essential structural and functional component of endothelial cells. Extensive hemodynamic changes cause endothelial glycocalyx disruption and vascular dysfunction, leading to multiple arterial and venous disorders. Chronic venous disease (CVD) is a common disorder of the lower extremities with major health and socio-economic implications, but complex pathophysiology.

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Tissue regeneration after a wound occurs through three main overlapping and interrelated stages namely inflammatory, proliferative, and remodelling phases, respectively. The inflammatory phase is key for successful tissue reconstruction and triggers the proliferative phase. The macrophages in the non-healing wounds remain in the inflammatory loop, but their phenotypes can be changed interactions with nanofibre-based scaffolds mimicking the organisation of the native structural support of healthy tissues.

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Schwann cells (SCs) hold key roles in axonal function and maintenance in the peripheral nervous system (PNS) and are a critical component to the regeneration process following trauma. Following PNS trauma, SCs respond to both physical and chemical signals to modify phenotype and assist in the regeneration of damaged axons and extracellular matrix (ECM). There is currently a lack of knowledge regarding the SC response to dynamic, temporal changes in the ECM brought on by swelling and the development of scar tissue as part of the body's wound-healing process.

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