scholarly journals Endoplasmic reticulum stress in lung disease

2017 ◽  
Vol 26 (144) ◽  
pp. 170018 ◽  
Author(s):  
Stefan J. Marciniak

Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease. These insights may offer opportunities to manipulate such endoplasmic reticulum stress pathways and thereby cure lung disease.

CHEST Journal ◽  
2013 ◽  
Vol 143 (4) ◽  
pp. 1098-1105 ◽  
Author(s):  
James Wei ◽  
Sadaf Rahman ◽  
Ehab A. Ayaub ◽  
Jeffrey G. Dickhout ◽  
Kjetil Ask

CHEST Journal ◽  
2020 ◽  
Vol 157 (5) ◽  
pp. 1207-1220 ◽  
Author(s):  
Safaa Naiel ◽  
Victor Tat ◽  
Manreet Padwal ◽  
Megan Vierhout ◽  
Olivia Mekhael ◽  
...  

2021 ◽  
pp. 1-10
Author(s):  
Vera Kovaleva ◽  
Mart Saarma

Parkinson’s disease (PD) pathology involves progressive degeneration and death of vulnerable dopamine neurons in the substantia nigra. Extensive axonal arborisation and distinct functions make this type of neurons particularly sensitive to homeostatic perturbations, such as protein misfolding and Ca2 + dysregulation. Endoplasmic reticulum (ER) is a cell compartment orchestrating protein synthesis and folding, as well as synthesis of lipids and maintenance of Ca2 +-homeostasis in eukaryotic cells. When misfolded proteins start to accumulate in ER lumen the unfolded protein response (UPR) is activated. UPR is an adaptive signalling machinery aimed at relieving of protein folding load in the ER. When UPR is chronic, it can either boost neurodegeneration and apoptosis or cause neuronal dysfunctions. We have recently discovered that mesencephalic astrocyte-derived neurotrophic factor (MANF) exerts its prosurvival action in dopamine neurons and in animal model of PD through the direct binding to UPR sensor inositol-requiring protein 1 alpha (IRE1α) and attenuation of UPR. In line with this, UPR targeting resulted in neuroprotection and neurorestoration in various preclinical PD animal models. Therefore, growth factors (GFs), possessing both neurorestorative activity and restoration of protein folding capacity are attractive as drug candidates for PD treatment especially their blood-brain barrier penetrating analogs and small molecule mimetics. In this review, we discuss ER stress as a therapeutic target to treat PD; we summarize the existing preclinical data on the regulation of ER stress for PD treatment. In addition, we point out the crucial aspects for successful clinical translation of UPR-regulating GFs and new prospective in GFs-based treatments of PD, focusing on ER stress regulation.


2013 ◽  
Vol 144 (2) ◽  
pp. 357-368.e9 ◽  
Author(s):  
Sumaira Z. Hasnain ◽  
Sharyn Tauro ◽  
Indrajit Das ◽  
Hui Tong ◽  
Alice C.–H. Chen ◽  
...  

Thorax ◽  
2016 ◽  
Vol 71 (Suppl 3) ◽  
pp. A44.3-A45
Author(s):  
H Parfrey ◽  
E Moseley ◽  
B Beardsley ◽  
J Knight ◽  
SJ Marciniak ◽  
...  

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