Link Between Endoplasmic Reticulum Stress And Lipid Metabolism In Metabolic And Neurodegenerative Diseases

1318 words - 6 pages

Metabolic diseases and neurodegenerative diseases (ND) are the hallmarks of modern health issues,
affecting millions of people worldwide. Even though these diseases have different phenotypic
manifestations and symptoms, they share many pathophysiological characteristics such as chronic
endoplasmic reticulum (ER) stress and the impairment of ER stress responses such as the unfolded
protein response (UPR) that cannot re-establish homeostasis. In other studies, the disturbance in lipid
metabolism in these diseases was also proven, noting that the majority of lipid metabolism in cells
happens in the ER. In this review, we will discuss the relationship between ER stress and lipid metabolism
that has been proposed in metabolic diseases, and the potential link between ER stress and lipid
metabolism in ND diseases that remains to be unveiled. Proving the existence of a link between ER stress
and lipid metabolism might be of great interest for the development of drugs that target not only single
pathways in ND like current drugs do, but aim to target the connection between the different pathways
responsible for the development of the disorders.
Introduction
Endoplasmic reticulum functions
In eukaryotic cells, endoplasmic reticulum (ER) is an
organelle responsible for many vital functions such as
the production of secretory proteins, their folding and
transport to the Golgi complex [1]*. The synthesis of
sterol and phospholipids (principal components of lipids
in biological membranes) also takes place in the ER:
Hence, the crucial role of ER in lipid metabolism and
composition in membranes. ER maintains lipid
homeostasis, which is important for normal functions of
cells ([2] and references cited therein)**.
Endoplasmic reticulum stress and
responses
ER stress is caused when any of its functions is
disturbed, some of the disturbances are such as
hyperglycemia, hyperlipidemia, inflammatory cytokines,
etc. There are two types of ER stress: acute and
chronic ER stress. The acute form is induced by
treatment with chemicals for a limited time (e.g.
tunicamycin, cholesterol, etc.). However, chronic ER
stress is characterized by the continuous presence of
stress inducers. ER homeostasis is not restored by the
ER stress responses such as the unfolded protein
response (UPR) which is impaired in chronic ER stress
[3]**.
When proteins are misfolded for one reason or
another, the ER tries to degrade them by the ERassociated
protein degradation (ERAD). However,
when the amount of unfolded proteins exceeds the
folding capacity of the ER, the ER is stressed and the
UPR is activated. The UPR induces the expression of
ER chaperones responsible for the proper folding of
proteins, regulates lipid metabolism, ERAD
components and attenuates protein synthesis to lessen
the excess on the ER [4]. The accumulation of
misfolded proteins in the ER induces the UPR through
three main pathways: IRE1, PERK, and ATF6 in order
to re-establish homeostasis in the ER (figure 1).
However, in...

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