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The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease
Hanne Leysen1, Deborah Walter1, Lore Clauwaert1
1Receptor Biology Laboratory, University of Antwerp, 2610 Wilrijk, Belgium.
Abstract:
During the aging process our body becomes less well equipped to deal with cellular stress, resulting in an increase in unrepaired damage. This causes varying degrees of impaired functionality and an increased risk of mortality. One of the most effective anti-aging strategies involves interventions that combine simultaneous glucometabolic support with augmented DNA damage protection/repair. Thus, it seems prudent to develop therapeutic strategies that target this combinatorial approach. Studies have shown that the ADP-ribosylation factor (ARF) GTPase activating protein GIT2 (GIT2) acts as a keystone protein in the aging process. GIT2 can control both DNA repair and glucose metabolism. Through in vivo co-regulation analyses it was found that GIT2 forms a close coexpression-based relationship with the relaxin-3 receptor (RXFP3). Cellular RXFP3 expression is directly affected by DNA damage and oxidative stress. Overexpression or stimulation of this receptor, by its endogenous ligand relaxin 3 (RLN3), can regulate the DNA damage response and repair processes. Interestingly, RLN3 is an insulin-like peptide and has been shown to control multiple disease processes linked to aging mechanisms, e.g., anxiety, depression, memory dysfunction, appetite, and anti-apoptotic mechanisms. Here we discuss the molecular mechanisms underlying the various roles of RXFP3/RLN3 signaling in aging and age-related disorders.
Insights
Aging impairs cellular repair and increases mortality. Combining glucose metabolism support with DNA repair, targeting the GIT2-RXFP3/RLN3 pathway, offers a promising anti-aging strategy for age-related diseases.
Area of Science:
- Molecular Biology
- Gerontology
- Metabolism
Background:
- Aging leads to increased cellular stress and unrepaired damage, impairing function and increasing mortality.
- Effective anti-aging strategies require combined glucometabolic support and DNA damage protection/repair.
- The protein GIT2 (ADP-ribosylation factor GTPase activating protein) is crucial in aging, regulating both DNA repair and glucose metabolism.
Purpose of the Study:
- To explore the molecular mechanisms of RXFP3/RLN3 signaling in aging and age-related disorders.
- To investigate the role of GIT2 in aging and its relationship with RXFP3.
- To understand how RLN3, an insulin-like peptide, influences aging-related conditions.
Main Methods:
- In vivo co-expression analyses to identify relationships between GIT2 and RXFP3.
- Investigating the impact of DNA damage and oxidative stress on cellular RXFP3 expression.
- Reviewing literature on RLN3's role in aging mechanisms and disease processes.
Main Results:
- GIT2 exhibits a strong coexpression relationship with RXFP3.
- Cellular RXFP3 expression is sensitive to DNA damage and oxidative stress.
- RLN3/RXFP3 signaling modulates DNA damage response and repair, and impacts aging-related conditions like anxiety, depression, and memory dysfunction.
Conclusions:
- The GIT2-RXFP3/RLN3 pathway is a key regulator in aging and age-related diseases.
- Targeting this pathway offers a potential therapeutic strategy for combating aging.
- RLN3/RXFP3 signaling presents a novel target for interventions in aging and associated pathologies.
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