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IntroductionThe mitral valve, one of the heart's four valves, regulates blood flow. These valves have flaps that open and close to direct blood properly through the heart and body. During each heartbeat, the flaps open for blood to pass through and seal shut to prevent backflow. Specifically, the mitral valve opens to allow blood flow from the heart's upper left chamber to the lower left chamber. It then closes securely as the lower left chamber contracts to pump blood to the body, preventing...
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Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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Related Experiment Video

Updated: Dec 7, 2025

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss
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Pathophysiological mechanisms underlying MAFLD.

Mohammad Shafi Kuchay1, Narendra Singh Choudhary2, Sunil Kumar Mishra1

  • 1Division of Endocrinology and Metabolism, Medanta the Medicity Hospital, Gurugram, 122001, Haryana, India.

Diabetes & Metabolic Syndrome
|September 30, 2020
PubMed
Summary
This summary is machine-generated.

Metabolic associated fatty liver disease (MAFLD) involves complex pathways. Understanding downstream mechanisms like inflammation and fibrosis, and factors like gut microbiome, is key for new MAFLD treatments.

Keywords:
Bone morphogenetic protein 8BExtracellular vesiclesFibroblast growth factor 19Metabolic associated fatty liver diseaseMetabolic associated steatohepatitisNASHNon-alcoholic fatty liver diseaseNotch pathwayTAZ/IHH pathway

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Gastroenterology

Background:

  • Metabolic associated fatty liver disease (MAFLD) pathogenesis involves insulin resistance, lipotoxicity, inflammation, and hepatic stellate cell (HSC) activation.
  • While initial processes are understood, downstream molecular mechanisms of inflammation, lipoapoptosis, and fibrogenesis remain unclear.

Purpose of the Study:

  • To review current literature on the pathophysiology of MAFLD.
  • To identify emerging concepts and potential therapeutic targets in MAFLD pathogenesis.

Main Methods:

  • A comprehensive literature search was conducted using Medline (PubMed), Scopus, and Google Scholar databases.
  • Keywords included "nonalcoholic fatty liver disease," "metabolic associated fatty liver disease," "nonalcoholic steatohepatitis," and "NASH pathogenesis."

Main Results:

  • Hepatic stellate cell (HSC) activation is a common endpoint, leading to extracellular matrix (ECM) accumulation and liver damage.
  • Key regulators of HSC activation include TAZ, hedgehog ligands, TGF-β, BMP8B, and osteopontin.
  • Factors like gut microbiome, bile acid metabolism, endogenous alcohol, and fructose handling influence MASH susceptibility.

Conclusions:

  • Emerging concepts in MAFLD pathophysiology include the TAZ/Ihh pathway, extracellular vesicles, microRNA, gut microbiome, and intestinal fructose metabolism.
  • These newer insights offer promising targets for developing novel therapeutic agents for MAFLD and MASH.