Abstract

Massive hepatic necrosis is the most severe lesion in acute liver failure, yet a portion of patients manage to survive and recover from this high-risk and harsh disease syndrome. The mechanisms underlying recovery remain largely unknown to date. Recent research progress highlights a key role of liver progenitor cells, the smallest biliary cells, in the maintenance of liver homeostasis and thus survival. These stem-like cells rapidly proliferate and take over crucial hepatocyte functions in a severely damaged liver. Hence, the new findings not only add to our understanding of the huge regenerative capability of the liver, but also provide potential new targets for the pharmacological management of acute liver failure in clinical practice.

Highlights

  • Introduction a Patient Survive Acute LiverThe current commonly accepted nomenclature of acute liver failure (ALF), with alternative terms including “fulminant hepatitis” and “fulminant hepatic failure”, was coined by Roger Williams and colleagues in 1993 [1]

  • Histological examination revealed that liver progenitor cells (LPC) in the surviving ALF patients showed robust p-SMAD2 immune positivity, whereas those in the irreversible patients did not

  • These results suggest that there is/are factor(s) inhibiting activin A signaling in LPC of the irreversible patients

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Summary

Introduction a Patient Survive Acute Liver

The current commonly accepted nomenclature of acute liver failure (ALF), with alternative terms including “fulminant hepatitis” and “fulminant hepatic failure”, was coined by Roger Williams and colleagues in 1993 [1]. Their ALF definition describes a severe liver injury leading to coagulation abnormality, usually with an international normalized ratio (INR) ≥1.5, and any degree of mental alteration (encephalopathy) in a patient without pre-existing liver disease and with an illness of up to 4 weeks of duration [1]. ALF included patients with pre-existing liver disease, those with chronic HBV infection [4]. The definitions of ALF, ACLF, EASL-ACLF, sepsis and sepsis in cirrhosis, are briefly discussed in an isolated section

Who Takes over Hepatocyte Functions to Support Systemic Homeostasis Following
How Do LPC Initiate Robust HNF4α Expression?
Disease Model: A Bottleneck in Studying the Mechanisms of Acute Liver Failure
Conclusions and Perspectives
Findings and Implications for Human

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