1. Recent advancement of molecular mechanisms of liver fibrosis.

    Journal of Hepato-Biliary-Pancreatic Sciences 22(7):512 (2015) PMID 25869468

    Liver fibrosis occurs in response to any etiology of chronic liver injury including hepatitis B and C, alcohol consumption, fatty liver disease, cholestasis, and autoimmune hepatitis. Hepatic stellate cells (HSCs) are the primary source of activated myofibroblasts that produce extracellular matr...
  2. Aging and liver disease.

    Current Opinion in Gastroenterology 31(3):184 (2015) PMID 25850346

    Aging is a condition in which a person gradually loses the ability to maintain homeostasis, due to structural alteration or dysfunction. Aging is a major risk factor for most chronic diseases. As the liver has a remarkable ability to regenerate, this review assessed the effect of aging on clinic...
  3. Ezetimibe for the treatment of nonalcoholic steatohepatitis: assessment by novel magnetic resonance imaging and magnetic resonance elastography in a randomized trial (MOZART trial).

    Hepatology 61(4):1239 (2015) PMID 25482832 PMCID PMC4407930

    Ezetimibe inhibits intestinal cholesterol absorption and lowers low-density lipoprotein cholesterol. Uncontrolled studies have suggested that it reduces liver fat as estimated by ultrasound in nonalcoholic steatohepatitis (NASH). Therefore, we aimed to examine the efficacy of ezetimibe versus pl...
  4. Commensal microbiota is hepatoprotective and prevents liver fibrosis in mice.

    FASEB Journal 29(3):1043 (2015) PMID 25466902

    Translocation of bacteria and their products across the intestinal barrier is common in patients with liver disease, and there is evidence that experimental liver fibrosis depends on bacterial translocation. The purpose of our study was to investigate liver fibrosis in conventional and germ-free...
  5. Commensal microbiota is hepatoprotective and prevents liver fibrosis in mice.

    FASEB Journal 29(3):1043 (2015) PMID 25466902 PMCID PMC4422368

    Translocation of bacteria and their products across the intestinal barrier is common in patients with liver disease, and there is evidence that experimental liver fibrosis depends on bacterial translocation. The purpose of our study was to investigate liver fibrosis in conventional and germ-free...
  6. Intestinal FXR agonism promotes adipose tissue browning and reduces obesity and insulin resistance.

    Nature Medicine 21(2):159 (2015) PMID 25559344 PMCID PMC4320010

    The systemic expression of the bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting cholesterol metabolism, triglyceride production, hepatic steatosis and biliary cholestasis. In contrast to systemic therapy, bile acid release during a meal selectively ac...
  7. Contribution of bone marrow-derived fibrocytes to liver fibrosis.

    Hepatobiliary surgery and nutrition 4(1):34 (2015) PMID 25713803 PMCID PMC4318956

    Since the discovery of fibrocytes in 1994 by Dr. Bucala and colleagues, these bone marrow (BM)-derived collagen Type I producing CD45(+) cells remain the most fascinating cells of the hematopoietic system. Despite recent reports on the emerging contribution of fibrocytes to fibrosis of parenchym...
  8. Contribution of bone marrow-derived fibrocytes to liver fibrosis.

    Hepatobiliary surgery and nutrition 4(1):34 (2015) PMID 25713803 PMCID PMC4318956

    Since the discovery of fibrocytes in 1994 by Dr. Bucala and colleagues, these bone marrow (BM)-derived collagen Type I producing CD45(+) cells remain the most fascinating cells of the hematopoietic system. Despite recent reports on the emerging contribution of fibrocytes to fibrosis of parenchym...
  9. Intestinal FXR agonism promotes adipose tissue browning and reduces obesity and insulin resistance.

    Nature Medicine 21(2):159 (2015) PMID 25559344

    The systemic expression of the bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting cholesterol metabolism, triglyceride production, hepatic steatosis and biliary cholestasis. In contrast to systemic therapy, bile acid release during a meal selectively ac...
  10. Intestinal FXR agonism promotes adipose tissue browning and reduces obesity and insulin resistance.

    Nature Medicine 21(2):159 (2015) PMID 25559344

    The systemic expression of the bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting cholesterol metabolism, triglyceride production, hepatic steatosis and biliary cholestasis. In contrast to systemic therapy, bile acid release during a meal selectively ac...
  11. Contribution of bone marrow-derived fibrocytes to liver fibrosis.

    Hepatobiliary surgery and nutrition 4(1):34 (2015) PMID 25713803

    Since the discovery of fibrocytes in 1994 by Dr. Bucala and colleagues, these bone marrow (BM)-derived collagen Type I producing CD45(+) cells remain the most fascinating cells of the hematopoietic system. Despite recent reports on the emerging contribution of fibrocytes to fibrosis of parenchym...
  12. Intestinal FXR agonism promotes adipose tissue browning and reduces obesity and insulin resistance.

    Nature Medicine 21(2):159 (2015) PMID 25559344 PMCID PMC4320010

    The systemic expression of the bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting cholesterol metabolism, triglyceride production, hepatic steatosis and biliary cholestasis. In contrast to systemic therapy, bile acid release during a meal selectively ac...
  13. Deficiency of NOX1 or NOX4 Prevents Liver Inflammation and Fibrosis in Mice through Inhibition of Hepatic Stellate Cell Activation.

    PLoS ONE 10(7):e0129743 (2015) PMID 26222337 PMCID PMC4519306

    Reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate oxidase (NOX) play a key role in liver injury and fibrosis. Previous studies demonstrated that GKT137831, a dual NOX1/4 inhibitor, attenuated liver fibrosis in mice as well as pro-fibrotic genes in hepatic stel...
  14. Agreement between TOAST and CCS ischemic stroke classification: The NINDS SiGN Study.

    Neurology 83(18):1653 (2014) PMID 25261504 PMCID PMC4223086

    The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems. Study subjects included 13,596 adult men and women accrued from 20 US and...
  15. Agreement between TOAST and CCS ischemic stroke classification: the NINDS SiGN study.

    Neurology 83(18):1653 (2014) PMID 25261504 PMCID PMC4223086

    The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems. Study subjects included 13,596 adult men and women accrued from 20 US and...
  16. Agreement between TOAST and CCS ischemic stroke classification: the NINDS SiGN study.

    Neurology 83(18):1653 (2014) PMID 25261504 PMCID PMC4223086

    The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems. Study subjects included 13,596 adult men and women accrued from 20 US and...
  17. Agreement between TOAST and CCS ischemic stroke classification: the NINDS SiGN study.

    Neurology 83(18):1653 (2014) PMID 25261504 PMCID PMC4223086

    The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems. Study subjects included 13,596 adult men and women accrued from 20 US and...
  18. Agreement between TOAST and CCS ischemic stroke classification: the NINDS SiGN study.

    Neurology 83(18):1653 (2014) PMID 25261504 PMCID PMC4223086

    The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems. Study subjects included 13,596 adult men and women accrued from 20 US and...
  19. Origin of myofibroblasts in the fibrotic liver in mice.

    PNAS 111(32):E3297 (2014) PMID 25074909 PMCID PMC4136601

    Hepatic myofibroblasts are activated in response to chronic liver injury of any etiology to produce a fibrous scar. Despite extensive studies, the origin of myofibroblasts in different types of fibrotic liver diseases is unresolved. To identify distinct populations of myofibroblasts and quantify...
  20. Origin of myofibroblasts in the fibrotic liver in mice.

    PNAS 111(32):E3297 (2014) PMID 25074909 PMCID PMC4136601

    Hepatic myofibroblasts are activated in response to chronic liver injury of any etiology to produce a fibrous scar. Despite extensive studies, the origin of myofibroblasts in different types of fibrotic liver diseases is unresolved. To identify distinct populations of myofibroblasts and quantify...