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Psychoneuroimmunology (PNI) is a multidisciplinary field that examines how psychological factors, particularly stress, interact with the immune system and impact physical health. Research in PNI has shown that chronic or traumatic stress can disrupt both the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These disruptions contribute to serious health conditions, including cardiovascular diseases.
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Stress is a multifaceted response to events perceived as challenging or threatening, highlighting physical, emotional, cognitive, and behavioral reactions. Physically, stress can lead to fatigue, sleep disruptions, and various health issues such as frequent colds, chest pains, and nausea. Emotionally, it can manifest as anxiety, depression, irritability, and anger triggered by both minor and major life events. Cognitively, it may result in difficulty in concentration, memory, and...
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Related Experiment Video

Updated: Dec 12, 2025

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium
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[ER stress and NAFLD].

Floriane Lachkar1, Alexandra Papaioannou1, Pascal Ferré1

  • 1Centre de recherches des Cordeliers, UMRS1128 Inserm, Sorbonne Université, 15 rue de l'École de Médecine, 75270 Paris cedex 06, France.

Biologie Aujourd'Hui
|August 11, 2020
PubMed
Summary
This summary is machine-generated.

Non-alcoholic fatty liver disease (NAFLD) involves endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). Chronic UPR activation drives NAFLD progression, offering therapeutic targets for liver disease.

Keywords:
ER stressUPRinflammationlipideslipidsobesityobésitéstress du réticulum endoplasmique

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Area of Science:

  • Hepatology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Non-alcoholic fatty liver disease (NAFLD) is a prevalent condition linked to obesity.
  • NAFLD spectrum includes steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC).
  • Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) activation are implicated in NAFLD pathogenesis.

Purpose of the Study:

  • To elucidate the mechanisms by which UPR contributes to NAFLD progression.
  • To explore potential pharmacological interventions targeting UPR-mediated pathological pathways in the liver.

Main Methods:

  • Review of existing literature on ER stress and UPR in NAFLD.
  • Analysis of molecular mechanisms linking UPR to hepatic lipid accumulation, inflammation, and cell death.
  • Identification of therapeutic strategies targeting UPR pathways.

Main Results:

  • Chronic ER stress and sustained UPR activation promote lipid accumulation in hepatocytes.
  • Continuous UPR signaling contributes to hepatic inflammation and hepatocyte death.
  • These factors are critical drivers for advancing NAFLD to severe liver disease stages.

Conclusions:

  • UPR plays a pivotal role in the transition from a healthy liver to NAFLD.
  • Targeting UPR pathways presents a promising therapeutic avenue for managing NAFLD and its complications.
  • Further research into UPR modulation could lead to novel treatments for liver disease.