Journal
CELLS
Volume 12, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/cells12010150
Keywords
apelin; ELABELA; APJ; apelinergic system; apoptosis
Categories
Ask authors/readers for more resources
The apelinergic system, consisting of apelin, ELABELA, and the apelin receptor APJ, plays a multifaceted role in various biological functions. This review focuses on the role of the apelinergic system in cell apoptosis and highlights the signaling pathways involved, such as PI3K, ERK1/2, AKT, AMPK, and PKA. Dysregulation of apoptosis can lead to pathological conditions, and the apelinergic system shows potential as a therapeutic target in various diseases.
The apelinergic system comprises two peptide ligands, apelin and ELABELA, and their cognate G-protein-coupled receptor, the apelin receptor APJ. Apelin is a peptide that was isolated from bovine stomach extracts; the distribution of the four main active forms, apelin-36, -17, -13, and pyr-apelin-13 differs between tissues. The mature form of ELABELA-32 can be transformed into forms called ELABELA-11 or -21. The biological function of the apelinergic system is multifaceted, and includes the regulation of angiogenesis, body fluid homeostasis, energy metabolism, and functioning of the cardiovascular, nervous, respiratory, digestive, and reproductive systems. This review summarises the mechanism of the apelinergic system in cell apoptosis. Depending on the cell/tissue, the apelinergic system modulates cell apoptosis by activating various signalling pathways, including phosphoinositide 3-kinase (PI3K), extracellular signal-regulated protein kinase (ERK1/2), protein kinase B (AKT), 5'AMP-activated protein kinase(AMPK), and protein kinase A (PKA). Apoptosis is critically important during various developmental processes, and any dysfunction leads to pathological conditions such as cancer, autoimmune diseases, and developmental defects. The purpose of this review is to present data that suggest a significant role of the apelinergic system as a potential agent in various therapies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available