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Unfolded Protein Response Signaling in Hepatic Stem Cell Activation in Liver Fibrosis Publisher Pubmed



Salimi Z1 ; Rostami M2 ; Milasi YE1 ; Mafi A1, 3 ; Raoufinia R4, 5 ; Kiani A6 ; Sakhaei F1 ; Ghezelbash B7 ; Butler AE8 ; Mohammadsadeghipour M9 ; Sahebkar A10, 11
Authors
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Authors Affiliations
  1. 1. Department of Clinical Biochemistry, School of Pharmacy & Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  3. 3. Nutrition and Food Security Research Center, Isfahan University of Medical Sciences, Isfa-han, Iran
  4. 4. Medical Genetics and Molecular Medicine Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  5. 5. Neyshabur University of Medical Sciences, Neyshabur, Iran
  6. 6. Department of Immunolo-gy, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  7. 7. Department of Immunology, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran
  8. 8. Research Department, Royal College of Sur-geons in Ireland, PO Box 15503, Adliya, Bahrain
  9. 9. Department of Clinical Biochemistry, Afzalipoor Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran
  10. 10. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
  11. 11. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

Source: Current Protein and Peptide Science Published:2024


Abstract

Frequent exposure to various external and internal adverse forces (stresses) disrupts cell protein homeostasis through endoplasmic reticulum (ER) capacity saturation. This process leads to the unfolded protein response (UPR), which aims to re-establish/maintain optimal cellular equilibrium. This complex mechanism is involved in the pathogenesis of various disorders, such as metabolic syndrome, fibrotic diseases, neurodegeneration, and cancer, by altering cellular metabolic changes integral to activating the hepatic stellate cells (HSCs). The development of hepatic fibrosis is one of the consequences of UPR activation. Therefore, novel therapies that target the UPR pathway effectively and specifically are being studied. This article covers the involvement of the UPR signaling pathway in cellular damage in liver fibrosis. Investigating the pathogenic pathways related to the ER/UPR stress axis that contribute to liver fibrosis can help to guide future drug therapy approaches. © 2024 Bentham Science Publishers.
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