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Phosphoproteomic Analyses of Circulating Platelets from Acute-on-Chronic Liver Failure Patients
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Acute-on-chronic liver failure (ACLF) is a syndrome with high short-term
mortality. Rapidly occurring or exacerbated thrombocytopenia which is
closely associated with adverse clinical outcomes has been frequently
observed in ACLF patients. Novel approaches are needed to clarify how
thrombocytopenia occurs and how platelet function is altered in ACLF
patients. Using phosphorylated proteomic approaches with circulating
platelets from five pairs of ACLF patients, we discovered that altered
proteins might compromise regulation of actin cytoskeleton in
circulating platelets from ACLF patients ceased within 28 days compared
with those who survived. To our knowledge, this study is the first to
examine the phosphoproteomic profile of circulating platelets in
patients with liver failure. This dataset will be helpful for further
elucidation of the mechanisms underlying thrombocytopenia and its
potential pathogenic roles in ACLF.
Title: Phosphoproteomic Analyses of Circulating Platelets from Acute-on-Chronic Liver Failure Patients
Description:
Acute-on-chronic liver failure (ACLF) is a syndrome with high short-term
mortality.
Rapidly occurring or exacerbated thrombocytopenia which is
closely associated with adverse clinical outcomes has been frequently
observed in ACLF patients.
Novel approaches are needed to clarify how
thrombocytopenia occurs and how platelet function is altered in ACLF
patients.
Using phosphorylated proteomic approaches with circulating
platelets from five pairs of ACLF patients, we discovered that altered
proteins might compromise regulation of actin cytoskeleton in
circulating platelets from ACLF patients ceased within 28 days compared
with those who survived.
To our knowledge, this study is the first to
examine the phosphoproteomic profile of circulating platelets in
patients with liver failure.
This dataset will be helpful for further
elucidation of the mechanisms underlying thrombocytopenia and its
potential pathogenic roles in ACLF.
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