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Published on: May 21, 2020
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GPCR systems coordinate cellular resilience against aging-associated stress
Tabitha Boeringer1, Mia Pardo1, Carter J Craig1
1Receptor Biology Lab, Department of Drug Discovery, Moffitt Cancer Center, Tampa, FL, United States.
Frontiers in Molecular Biosciences
|April 23, 2026
Summary
Cellular damage causes aging diseases, but G protein-coupled receptors (GPCRs) help resilience. Stable GPCR complexes, called receptorsomes, act as hubs to sense and mitigate stress, potentially delaying aging pathologies.
Area of Science:
- Cellular biology
- Molecular medicine
- Aging research
Background:
- Aging is linked to cumulative cellular damage from various stressors.
- G protein-coupled receptors (GPCRs) are crucial for cellular stress resilience.
- Existing research highlights GPCRs' role in cellular defense mechanisms.
Purpose of the Study:
- To introduce the concept of "receptorsomes" as stable GPCR complexes.
- To explore how receptorsomes integrate and mitigate stress across cellular compartments.
- To link receptosome composition to aging hallmarks and stress responses.
Main Methods:
- Literature review synthesizing evidence on GPCR complexes and stress.
- Analysis of receptosome composition and its role in cellular resilience.
- Mapping receptosome functions to specific aging hallmarks and stress types (oxidative, proteostatic, hypoxic).
Main Results:
- Receptorsomes are proposed as adaptive hubs comprising GPCRs and specific adaptors (e.g., β-arrestins, GIT2, RGS proteins, ASK1, YAP/TAZ).
- These complexes enable G protein-independent signaling for stress detection, damage repair, and homeostasis.
- Receptosome composition is linked to cellular responses against diverse stressors relevant to aging.
Conclusions:
- Receptorsomes represent a novel framework for understanding cellular adaptation to stress.
- Therapeutic modulation of receptosome adaptors may enhance resilience and health span.
- Targeting receptorsomes offers a potential strategy to delay age-related diseases and promote longevity.
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