Liver injury during highly pathogenic human coronavirus infections

Ling Xu, Jia Liu, Mengji Lu, Dongliang Yang, Xin Zheng – 14 March 2020 – The severe acute respiratory syndrome coronavirus 2 (SARS‐Cov‐2), the pathogen of 2019 novel coronavirus disease (COVID‐19), has posed a serious threat to global public health. The WHO has declared the outbreak of SARS‐CoV‐2 infection an international public health emergency. Lung lesions have been considered as the major damage caused by SARS‐CoV‐2 infection. However, liver injury has also been reported to occur during the course of the disease in severe cases.

Liver injury during highly pathogenic human coronavirus infections

Ling Xu, Jia Liu, Mengji Lu, Dongliang Yang, Xin Zheng – 14 March 2020 – The severe acute respiratory syndrome coronavirus 2 (SARS‐Cov‐2), the pathogen of 2019 novel coronavirus disease (COVID‐19), has posed a serious threat to global public health. The WHO has declared the outbreak of SARS‐CoV‐2 infection an international public health emergency. Lung lesions have been considered as the major damage caused by SARS‐CoV‐2 infection. However, liver injury has also been reported to occur during the course of the disease in severe cases.

Genetic Pathways in Nonalcoholic Fatty Liver Disease: Insights From Systems Biology

Silvia Sookoian, Carlos J. Pirola, Luca Valenti, Nicholas O. Davidson – 14 March 2020 – Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide epidemic whose etiology reflects multiple interactions between environmental and genetic factors. Here, we review the major pathways and dominant genetic modifiers known to be relevant players in human NAFLD and which may determine key components of the heritability of distinctive disease traits including steatosis and fibrosis.

Genetic Pathways in Nonalcoholic Fatty Liver Disease: Insights From Systems Biology

Silvia Sookoian, Carlos J. Pirola, Luca Valenti, Nicholas O. Davidson – 14 March 2020 – Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide epidemic whose etiology reflects multiple interactions between environmental and genetic factors. Here, we review the major pathways and dominant genetic modifiers known to be relevant players in human NAFLD and which may determine key components of the heritability of distinctive disease traits including steatosis and fibrosis.

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