Figure 1 NAFLD pathogenesis

Slides:

Advertisements

Similar presentations

Non-alcoholic Fatty Liver Disease

Advertisements

Figure 1 Proposed risk stratification for patients with NAFLD

Samir Parekh, Frank A. Anania Gastroenterology

Nutritional therapy for nonalcoholic fatty liver disease

Intermyocellular fat depot

Figure 2 Inflammatory pathways affecting hepatic insulin resistance

Bin Gao, Hidekazu Tsukamoto Gastroenterology

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

From Fat to Inflammation

More Than Meets the Eye: Identifying Who Is at Risk for NASH

Figure 3 Extracellular stimuli to HSC activation

Figure 5 Dendritic cells in liver inflammation

Figure 1 Contribution of the gut microbiota

Genetics and epigenetics of NAFLD and NASH

How to Approach a Patient With Nonalcoholic Fatty Liver Disease

Figure 1 Pathophysiological aspects of insulin

Figure 2 A stage-based approach to the treatment of NAFLD

T. Vescovo, G. Refolo, G. Vitagliano, G.M. Fimia, M. Piacentini

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nonalcoholic steatohepatitis

Fatty Acid-Induced T Cell Loss Greases Liver Carcinogenesis

Samir Parekh, Frank A. Anania Gastroenterology

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Features, Diagnosis, and Treatment of Nonalcoholic Fatty Liver Disease

Figure 6 Combination therapy for HCC

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 4 Proinflammatory immune cells and their crosstalk in patients with IBD Figure 4 | Proinflammatory immune cells and their crosstalk in patients.

Roles for Chemokines in Liver Disease

Figure 1 Definition and concept of ACLF

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Functions, features and phenotypes of HSCs in normal and diseased livers Figure 1 | Functions, features and phenotypes of HSCs in normal and diseased.

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

NAFLD: A multisystem disease

Figure 3 The mechanism of injury in ACLF

Volume 55, Issue 4, Pages (October 2011)

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

to the liver and promote patient-derived xenograft tumour growth

Figure 1 Environmental factors contributing to IBD pathogenesis

Figure 2 Organ crosstalk in the pathophysiology

Figure 3 Clinical algorithms in the management of NASH and diabetes mellitus Figure 3 | Clinical algorithms in the management of NASH and diabetes mellitus.

Sugar, Sugar Not So Sweet for the Liver

Example of algorithm for clinical assessment of patients at risk of non-alcoholic fatty liver disease Example of algorithm for clinical assessment.

I. Carmona, P. Cordero, J. Ampuero, A. Rojas, M. Romero-Gómez

Amalia Gastaldelli, Giulio Marchesini Journal of Hepatology

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 2 Three distinct paracellular epithelial

Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets

Figure 1 Key mechanistic pathways involved in the gut–liver axis in NAFLD progression Figure 1 | Key mechanistic pathways involved in the gut–liver axis.

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 6 Possible therapeutic targets to decrease hepatic steatosis

Figure 2 Schematic of normal and abnormal liver regeneration

Figure 1 Animal models of liver regeneration

Autophagy: A Sweet Process in Diabetes

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 3 Strategies to improve liver regeneration

Figure 7 T cells in liver inflammation

Figure 6 Innate lymphoid cells in liver inflammation

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

NASH animal models: Are we there yet?

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 3 Bile acid-induced hepatic inflammation and carcinogenesis

Figure 2 Lifelong influences on the gut microbiome from

Molecular mechanism of PPARα action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease Michal Pawlak,

How to Approach a Patient With Nonalcoholic Fatty Liver Disease

Volume 135, Issue 6, Pages (December 2008)

Presentation transcript:

Figure 1 NAFLD pathogenesis Figure 1 | NAFLD pathogenesis. A combination of genetic factors and environmental factors can influence hepatic steatosis risk. In patients with hepatic steatosis, inflammation is triggered by multiple mechanisms. These processes activate Kuppfer cells and stellate cells, and promote a type 2 T helper (TH2) cell inflammatory response, with progressive fibrosis. NASH can progress to cirrhosis. Hepatocellular carcinoma (HCC) often occurs in the context of NASH cirrhosis but can occur without cirrhosis. Inhibition of activated CD8+ T cells and increased cell proliferation confer increased HCC risk. DNL, de novo lipogenesis; FFA, free fatty acids; IR, insulin resistance; JNK1, c-Jun N-terminal kinase 1; ROS, reactive oxygen species. Khan, R. S. & Newsome, P. N. (2018) Novel insights into mechanisms of disease progression Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.181