Endoplasmic reticulum and the microRNA environment in the cardiovascular system

Abstract

Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in the biology of the cardiac myocyte, and are involved in pathological cardiac function and remodeling. In this paper, we review a link between endoplasmic reticulum homeostasis and microRNA with an emphasis on the impact on stress responses in the cardiovascular system.

Calreticulin and the Heart

“…miRNA plays a significant role in cardiovascular differentiation, function, and disease and has been the target of intense scrutiny [ 19 , 20 , 21 ]. Ingenuity Pathway Analysis of miRNA that was identified in calreticulin-deficient ES cells indicates that the top canonical pathways affected in the absence of calreticulin are Wnt signaling, TGFβ signaling, and cardiac hypertrophy markers ( Table 1 ).…”

Crosstalk between endoplasmic reticulum stress and non‐coding RNAs in cardiovascular diseases

“…The inability to respond to cellular stress may result in cell death. To mitigate cellular stress and restore homeostasis, cells within the cardiovascular system, including cardiomyocytes, vascular endothelial cells, and vascular smooth muscle cells, could activate stress coping‐response mechanisms (Groenendyk et al, 2013; Groenendyk et al, 2019). Three distinct signaling pathways can induce the UPR in mammalian cells, namely inositol‐requiring enzyme 1 (IRE1), protein kinase R‐like ER kinase (PERK), and activating transcription factor (ATF6).…”