Multi-organ Linkage Pathophysiology and Therapy for NAFLD and NASH

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86

authors

12

articles

Multi-organ Linkage Pathophysiology and Therapy for NAFLD and NASH

37.3K

views

86

authors

12

articles

Editorial

05 June 2024

Editorial: Multi-organ linkage pathophysiology and therapy for NAFLD and NASH

Takefumi Kimura

,

Tomoo Yamazaki

and

Gabriel Rufino Estrela

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NAFLD and NASH refer to the hepatic phenotype of metabolic syndromes strongly associated with obesity, diabetes, and dyslipidemia. NAFLD and NASH have complex pathogenesis modulated not only by the liver but also by muscle, adipose tissue, pancreas, gut microbiome, and immune and central nervous systems. This complex pathology, coupled with insulin resistance, lipid and bile acid changes, and congenital genetic predisposition, induces liver injury due to oxidative stress, endoplasmic reticulum stress, and autophagy dysfunction. Additionally, NAFLD and NASH contribute to diseases such as cirrhosis, atherosclerosis, chronic kidney disease, lung disease, and cancer in various organs, leading to systemic multi-organ damage. Even though enthusiastic development of new drugs for NAFLD and NASH has been underway, we are still lacking progress in generating therapeutic agents based on multiorgan-related pathomechanisms. In this special issue, we welcome clinical and basic studies on extrahepatic lesions as well as new findings related to liver pathology in NAFLD and NASH. Topic Editors welcome manuscripts particularly focusing on new therapies and new signaling pathways on the multiorgan-linkage of NAFLD and NASH.

NAFLD and NASH refer to the hepatic phenotype of metabolic syndromes strongly associated with obesity, diabetes, and dyslipidemia. NAFLD and NASH have complex pathogenesis modulated not only by the liver but also by muscle, adipose tissue, pancreas, gut microbiome, and immune and central nervous systems. This complex pathology, coupled with insulin resistance, lipid and bile acid changes, and congenital genetic predisposition, induces liver injury due to oxidative stress, endoplasmic reticulum stress, and autophagy dysfunction. Additionally, NAFLD and NASH contribute to diseases such as cirrhosis, atherosclerosis, chronic kidney disease, lung disease, and cancer in various organs, leading to systemic multi-organ damage. Even though enthusiastic development of new drugs for NAFLD and NASH has been underway, we are still lacking progress in generating therapeutic agents based on multiorgan-related pathomechanisms. In this special issue, we welcome clinical and basic studies on extrahepatic lesions as well as new findings related to liver pathology in NAFLD and NASH. Topic Editors welcome manuscripts particularly focusing on new therapies and new signaling pathways on the multiorgan-linkage of NAFLD and NASH.

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Frontiers in Endocrinology

Frontiers in Public Health

Frontiers in Nutrition

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