Publications by authors named "Sarah Calabro"
Article Synopsis
- - Chronic liver inflammation leads to severe conditions like fibrosis and cirrhosis, and the study identifies the glycoprotein CD147 as a crucial player in this process by influencing the formation of leukocyte aggregates.
- - Researchers examined liver samples using a specific antibody for CD147 and found that leukocyte clusters, or aggregates, contribute significantly to the severity of liver damage, and blocking CD147 reduced the size and number of these aggregates without affecting overall leukocyte count.
- - The findings suggest that CD147-mediated leukocyte aggregation is a key factor in liver injury development, occurring before traditional injury signs emerge, indicating its potential as a therapeutic target in preventing liver damage.
Hepatocytes in liver injury: Victim, bystander, or accomplice in progressive fibrosis?
J Gastroenterol Hepatol
December 2015
Chronic liver disease causes significant morbidity and mortality through progressive fibrosis, cirrhosis, and liver cancer. The classical theory of fibrogenesis has hepatic stellate cells (HSCs) as the principal and only significant source of abnormal extracellular matrix (ECM). Further, HSCs have the major role in abnormal ECM turnover.
View Article and Find Full Text PDFBackground: The classical paradigm of liver injury asserts that hepatic stellate cells (HSC) produce, remodel and turnover the abnormal extracellular matrix (ECM) of fibrosis via matrix metalloproteinases (MMPs). In extrahepatic tissues MMP production is regulated by a number of mechanisms including expression of the glycoprotein CD147. Previously, we have shown that CD147 is expressed on hepatocytes but not within the fibrotic septa in cirrhosis [1].
View Article and Find Full Text PDFBackground & Aims: In vertebrates, canonical Hedgehog (Hh) pathway activation requires Smoothened (SMO) translocation to the primary cilium (Pc), followed by a GLI-mediated transcriptional response. In addition, a similar gene regulation occurs in response to growth factors/cytokines, although independently of SMO signalling. The Hh pathway plays a critical role in liver fibrosis/regeneration, however, the mechanism of activation in chronic liver injury is poorly understood.
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