G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence
Paula Santos-Otte1, Hanne Leysen2,3, Jaana van Gastel2,3
1Center for Molecular and Cellular Bioengineering (CMCB), Technische Universität Dresden, 01062 Dresden, Germany.
Computational and Structural Biotechnology Journal
|January 11, 2020
Summary
Cellular senescence, a hallmark of aging, is linked to age-related diseases. G-protein-coupled receptors (GPCRs) may offer a therapeutic target to control senescence and combat aging disorders.
Area of Science:
- Gerontology
- Molecular Biology
- Cell Biology
Background:
- Aging is a primary risk factor for neurodegenerative, cancer, and cardiovascular diseases.
- Age-related diseases stem from declining intercellular communication, reduced receptor signaling efficiency, and increased apoptosis and cellular senescence.
- Cellular senescence, a key aging hallmark, contributes to age-related disorders.
Purpose of the Study:
- To explore the role of G-protein-coupled receptors (GPCRs) in cellular senescence.
- To investigate GPCRs as potential therapeutic targets for age-related diseases.
Main Methods:
- Review of recent advances in GPCR signaling.
- Analysis of emerging data on GPCR involvement in cellular senescence.
Main Results:
- GPCRs are crucial for cell signaling in nearly all physiological processes.
- Emerging evidence implicates GPCRs and associated proteins in the development of cellular senescence.
- GPCRs represent a promising therapeutic avenue for controlling cellular senescence.
Conclusions:
- GPCRs are integral to cellular signaling and implicated in aging.
- Targeting GPCRs could provide a novel strategy to manage cellular senescence.
- GPCR-targeted therapies hold potential for treating age-related disorders.
Keywords:
ADP-ribosylation factor GTPase-activating protein, (Arf-GAP)AT1R blockers, (ARB)AgingAngiotensin II, (Ang II)Ataxia telangiectasia mutated, (ATM)Cellular senescenceG protein-coupled receptor kinase interacting protein 2 (GIT2)G protein-coupled receptor kinase interacting protein 2, (GIT2)G protein-coupled receptor kinase, (GRK)G protein-coupled receptors (GPCRs)G protein-coupled receptors, (GPCRs)Hutchinson–Gilford progeria syndrome, (HGPS)Lysophosphatidic acid, (LPA)Regulator of G-protein signaling, (RGS)Relaxin family receptor 3, (RXFP3)active state, (R*)angiotensin type 1 receptor, (AT1R)angiotensin type 2 receptor, (AT2R)beta2-adrenergic receptor, (β2AR)cyclin-dependent kinase 2, (CDK2)cyclin-dependent kinase inhibitor 1, (cdkn1A/p21)endothelial cell differentiation gene, (Edg)inactive state, (R)latent semantic indexing, (LSI)mitogen-activated protein kinase, (MAPK)nuclear factor kappa-light-chain-enhancer of activated B cells, (NF- κβ)protein kinases, (PK)purinergic receptors family, (P2Y)renin-angiotensin system, (RAS)retinoblastoma, (RB)senescence associated secretory phenotype, (SASP)stress-induced premature senescence, (SIPS)transcription factor E2F3, (E2F3)transmembrane, (TM)tumor suppressor gene PTEN, (PTEN)tumor suppressor protein 53, (p53)vascular smooth muscle cells, (VSMC)β-ArrestinRelated Concept Videos
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