ArticleThe journal of cardiovascular aging2021
Ser9 phosphorylation of GSK-3β promotes aging in the heart through suppression of autophagy.
Article in The journal of cardiovascular aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Isoginkgetin protects against degeneration of ALS motor neurons via regulating the GSK-3β-TFEB signaling axis.Pharmacological research · 2026Article
- Panx1 deficiency exacerbates GAN diet-induced obesity by destabilizing β-catenin via GSK3β.iScience · 2026Article
- Enhancing Ulk1-Ser913 Phosphorylation as a Novel Therapy for Cardiac Aging.Journal of cardiovascular translational research · 2025Article
- S913 phosphorylation of Ulk1 protects the heart from aging through inhibition of cardiac senescence.Cardiovascular research · 2025Article
- Vascular inflammaging: Endothelial CEACAM1 expression is upregulated by TNF-α via independent activation of NF-κB and β-catenin signaling.Aging cell · 2025Article
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- GSK-3 at the heart of cardiometabolic diseases: Isoform-specific targeting is critical to therapeutic benefit.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Alleviating effect of lycorine on CFA‑induced arthritic pain via inhibition of spinal inflammation and oxidative stress.Experimental and therapeutic medicine · 2023Article
- YAP/TAZ dull the STING of aging.The journal of cardiovascular aging · 2022Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionGlycogen synthase kinase-3β (GSK-3β) is a serine/threonine kinase and a negative regulator of cardiac hypertrophy. Phosphorylation of GSK-3β at Ser9 negatively regulates its kinase activity. The role of GSK-3β in cardiac aging remains poorly understood.
aimThe study aimed to elucidate the role of GSK-3β Ser9 phosphorylation in mediating cardiac aging and the underlying mechanism. METHODS AND
resultsPhosphorylation of GSK-3β at Ser9 and the levels of β-catenin and Mcl-1 were increased in the mouse heart during aging, suggesting that GSK-3β is inactivated during aging in the heart. Age-induced cardiac hypertrophy, fibrosis, left ventricular dysfunction, and increases in cardiomyocyte apoptosis and senescence were all attenuated in constitutively active GSK-3β
conclusionOur results suggest that GSK-3β is inactivated during aging through Ser9 phosphorylation, which in turn plays an important role in mediating cardiac aging. GSK-3β promotes autophagy through phosphorylation of Ulk1 at Ser913, which in turn prevents aging in the heart.
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