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您的检索式：作者名="DON C.ROCKEY"
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| 1 | The cellular microenvironment and cytoskeletal actin dynamics in liver fibrogenesis显示文摘Hepatic stellate cells(HSCs)are the primary effector cells in liver fibrosis.In the normal liver,HSCs serve as the primary vitamin A storage cells in the body and retain a“quiescent”phenotype.However,after liver injury,they transdifferentiate to an“activated”myofibroblast-like phenotype,which is associated with dramatic upregulation of smooth muscle specific actin and extracellular matrix proteins.The result is a fibrotic,stiff,and dysfunctional liver.Therefore,understanding the molecular mechanisms that govern HSC function is essential for the development of anti-fibrotic medications.The actin cytoskeleton has emerged as a key component of the fibrogenic response in wound healing.Recent data indicate that the cytoskeleton receives signals from the cellular microenvironment and translates them to cellular function—in particular,increased type I collagen expression.Dynamic in nature,the actin cytoskeleton continuously polymerizes and depolymerizes in response to changes in the cellular microenvironment.In this viewpoint,we discuss the recent developments underlying cytoskeletal actin dynamics in liver fibrosis,including how the cellular microenvironment affects HSC function and the molecular mechanisms that regulate the actininduced increase in collagen expression typical of activated HSCs. | NOUR HIJAZI DON C.ROCKEY ZENGDUN SHI | 2022 | BIOCELL2022，46，9： | 2 |
| 2 | The launch of Portal Hypertension&Cirrhosis in discovery and patient care显示文摘Cirrhosis represents the body's wound healing response to liver injury,is analogous to wound healing in other parenchymal organs,1 and is associated with portal hypertension.Indeed,portal hypertension represents the major complication of cirrhosis and is tightly linked to clinical outcomes in patients with cirrhosis.In fact,of all the clinical variables used to predict outcomes in patients with cirrhosis,the hepatic venous pressure gradient(HVPG)is arguably the best.However,the measurement of HVPG is considered to be an invasive procedure and requires specific expertise. | Don C.Rockey | 2022 | Portal Hypertension & Cirrhosis2022，1，2： | 0 |
| 3 | The natural history of patients with compensated cirrhosis and elevated hepatic venous pressure gradient显示文摘Aims:Portal hypertension is a major complication of liver cirrhosis.Hepatic venous pressure gradient(HVPG)appears to be one of the best surrogates of clinical outcomes.However,the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear.Methods:We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018.Of these,we identified and analyzed 20 patients with HVPG>12 mmHg without evidence of clinical decompensation(defined as ascites,nonbleeding esophageal varices or bleeding esophageal varices,hepatic encephalopathy,hepatopulmonary syndrome,or hepatic hydrothorax).Additionally,we compared this group to 40 randomly selected cirrhotic patients with HVPG>12 mmHg with signs of clinical decompensation.Clinical events were subsequently assessed(mean=33 months)after HVPG measurement.Results:Patients with high HVPG without evidence of clinical decompensation had a significantly lower model for end‐stage liver disease(MELD)scores(8±4)compared to decompensated patients(13±8,p=0.05).HVPG measurements were similar in compensated(17±6 mmHg)and decompensated(18±4 mmHg)patients.Over follow‐up for 33 months,8/20 compensated patients had a decompensating event and neither MELD(8 and 8,respectively)nor HVPG(17 and 18 mmHg,respectively)differentiated patients who remained compensated versus those that decompensated.Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event(3.5 vs.2.6 g/dl,respectively,p=0.05).Conclusions:A small,unique,population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long‐term follow‐up. | Andrew Wortham Ali Khalifa Don C.Rockey | 2022 | Portal Hypertension & Cirrhosis2022，1，2： | 0 |
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