ArticleBMC infectious diseases2025
Profiles of PCSK9, SREBP-2, and histopathology in COVID-19 and non-COVID-19 critical illness.
Article in BMC infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSevere illness caused by SARS-CoV-2 infection is associated with dysregulated cholesterol homeostasis. Proprotein convertase subtilisin/kexin type 9 (PCSK9), which regulates serum cholesterol levels, is induced in the plasma of patients with severe SARS-CoV-2 infection, compared to critically ill patients with other conditions. PCSK9 is primarily expressed in the liver, which is susceptible to damage during severe illness. Sterol regulatory element-binding protein 2 (SREBP-2) regulates PCSK9 expression, and higher activity of both PCSK9 and SREBP-2 is associated with liver injury and inflammation.
methodsLiver tissues from 20 COVID-19 and 20 pre-pandemic autopsy cases were analysed, matched for age, sex, and intensive care treatment. Hepatic PCSK9 and SREBP-2 protein levels were assessed via immunohistochemistry. Histological scores for steatosis, fibrosis, and cholestasis were recorded. Additionally, plasma SREBP-2 levels were measured by ELISA in 25 septic COVID-19 and 34 septic non-COVID-19 patients.
resultsAcross all cases, hepatocellular PCSK9 protein level was increased in the presence of cholestasis and positively correlated with hepatic SREBP-2 expression. No significant differences were observed between the COVID-19 and control groups regarding liver histology or hepatic PCSK9 and SREBP-2 protein levels. Plasma SREBP-2 levels were similar between COVID-19 and non-COVID-19 septic patients. Correlation analysis revealed positive associations between plasma SREBP-2, plasma PCSK9, and cholesteryl ester levels in the entire cohort, suggesting preserved SREBP-2 function during critical illness. Laboratory measures of liver disease in patients with and without SARS-CoV-2 infection were similar.
conclusionCritically ill patients with and without SARS-CoV-2 infection exhibit comparable hepatic expression of PCSK9 and SREBP-2, as well as similar liver histology and comparable levels of aminotransferases, bilirubin, and gamma-glutamyl transferase, which suggests that SARS-CoV-2 does not directly cause liver injury. As our cohort was small, this suggestion needs to be confirmed by studying larger groups.
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