Although the field of cardiac regeneration is relatively young, it is progressing rapidly with technological advancements. Genome editing tools are allowing researchers to creatively influence signaling pathways to be able to shed light on them and are important for addressing certain issues and limitations associated with in vitro and in vivo aspects of cardiac regeneration, such as imaging and immune rejection. In this chapter, the pathways involved in cardiac regeneration will be highlighted, and the role of gene-editing tools in endogenous and exogenous approaches to regenerate injured myocardium is discussed.
View Article and Find Full Text PDFThis case report describes an initially stabilized transcatheter heart valve that embolized in the ascending aorta, leading to a postprocedural acute type A aortic dissection.
View Article and Find Full Text PDFThe host response to COVID-19 pathophysiology over the first few days of infection remains largely unclear, especially the mechanisms in the blood compartment. We report on a longitudinal proteomic analysis of acute-phase COVID-19 patients, for which we used blood plasma, multiple reaction monitoring with internal standards, and data-independent acquisition. We measured samples on admission for 49 patients, of which 21 had additional samples on days 2, 4, 7, and 14 after admission.
View Article and Find Full Text PDFEur J Cardiothorac Surg
November 2021
Intracardiac cement embolism after percutaneous vertebroplasty is a rare, but dangerous, complication, and guiding principles for its management are not well described. The management of this present case of intracardiac cement embolism offers insight to facilitate the treatment decision-making process in symptomatic patients requiring extraction.
View Article and Find Full Text PDFVascular anomalies, including local and peripheral thrombosis, are a hallmark of glioblastoma (GBM) and an aftermath of deregulation of the cancer cell genome and epigenome. Although the molecular effectors of these changes are poorly understood, the upregulation of podoplanin (PDPN) by cancer cells has recently been linked to an increased risk for venous thromboembolism (VTE) in GBM patients. Therefore, regulation of this platelet-activating protein by transforming events in cancer cells is of considerable interest.
View Article and Find Full Text PDFCancer-associated thrombosis (CAT) is a morbid, potentially life threatening and biologically impactful paraneoplastic state. At least in part, CAT is likely driven by cancer-specific mechanisms the nature of which is still poorly understood, hampering diagnostic, prophylactic and therapeutic efforts. It is increasingly appreciated that cancer-specific drivers of CAT include a constellation of oncogenic mutations and their superimposed epigenetic states that shape the transcriptome, phenotype and secretome of cancer cell populations, including the repertoire of genes impacting the vascular and coagulation systems.
View Article and Find Full Text PDFThere are emerging linkages between biological and genetic aspects of cancer progression and the mechanisms of cancer-associated thrombosis. It is argued that reciprocal influences between cancer cells, their associated vascular stroma, and the hemostatic system may shape the mechanism of coagulopathy. In this regard, glioblastoma multiforme offers a paradigm where the prevalent occurrence of local microthrombosis and peripheral venous thromboembolism can be linked to the profiles of oncogenic driver mutations and their impact on the expression of coagulation-related genes (coagulome).
View Article and Find Full Text PDFMolecular profiling of human cancers revealed a startling diversity in disease-causing mechanisms superseding histological and anatomical commonalities. The emerging molecular subtypes and disease entities are often driven by distinct oncogenic pathways and their effectors, including those acting extracellularly on the vascular and coagulation systems. Indeed, several oncogenic mutations such as those affecting protein-coding genes (RAS, EGFR, PTEN, TP53) and non-coding RNA (microRNA) regulate multiple effectors of the coagulation system (coagulome), including tissue factor, protease activated receptors, clotting factors, mediators of platelet function and fibrinolysis.
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