1,721,144 research outputs found

    The Role of PAR2 in MASLD Progression and HCC Development

    No full text
    Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently become the leading cause of chronic liver disease and can progress to hepatocellular carcinoma (HCC) through multiple pathogenic mechanisms. Protease-activated receptor 2 (PAR2) is a G-protein-coupled receptor activated by proteases such as trypsin, tryptase or coagulation factors VII and Xa. Recent studies have shown that PAR2 expression is increased in the liver of patients with MASLD or liver fibrosis. Its activation is linked to metabolic dysfunction through several pathways, including SREBP1c activation, AMPK inhibition and Akt-induced insulin resistance. Inhibition of PAR2 has been effective in reducing MASLD progression in different animal models. Notably, PAR2 blockade has also been effective in more advanced stages of the disease by dampening chronic inflammation and fibrogenesis through the inhibition of hepatic stellate cell activation and of TGF-β and SerpinB3 production. PAR2 also plays a role in cancer development, promoting tumour proliferation, angiogenesis and expression of immune checkpoint inhibitors (like PD-L1, CD47 and CD24). Due to its multifaceted involvement in liver disease, PAR2 is emerging as a key therapeutic target in this clinical context. This review aims to summarise current knowledge on PAR2′s role in MASLD and its potential as a therapeutic target

    Going Beyond Counting First Authors in Author Co-citation Analysis

    Full text link
    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    La cardiomiopatia cirrotica.

    No full text
    I pazienti affetti da cirrosi epatica possono sviluppare una cardiopatia, alla quale si è dato il nome di “cardiomiopatia cirrotica”. Essa consiste in una disfunzione cardiaca cronica caratterizzata da: 1) incremento della gittata cardiaca; 2) disfunzione diastolica correlata ad un alterato rilascio diastolico a riposo; 3) ridotta contrattilità miocardica sotto stimolo; 4) anormalità elettrofisiologiche, in assenza di malattia cardiaca organica accertata. La cardiomiopatia cirrotica è, di solito, subclinica e può essere riconosciuta solo attraverso il riscontro di alterazioni eco- e/o elettrocardiografiche. Tuttavia, essa può slatentizzarsi in occasione di eventi stressanti, quali emorragie digestive, infezioni batteriche, chirurgia maggiore, applicazione di shunt porto-cavale intraepatico transgiugulare [TIPS], od a seguito della somministrazione di farmaci vasocostrittori, situazioni che possono indurre un brusco incremento del lavoro cardiaco. Anche se non frequentemente, dopo trapianto di fegato od applicazione di TIPS è stata descritta l’insorgenza di insufficienza cardiaca conclamata, che rappresenta una causa di decesso in questi contesti. Infine, la presenza di cardiomiopatia cirrotica sembra avere un valore prognostico ai fini della sopravvivenza, che se questo aspetto non è stato ancora compiutamente definito
    corecore