ArticleMetabolism: clinical and experimental2019
Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase.
Article in Metabolism: clinical and experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Catalytic lactate-regulatory nanosystems attenuate cellular senescence for atherosclerosis amelioration.Bioactive materials · 2026Article
- LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.Circulation research · 2026Article
- The role of ubiquitin system in ageing-related diseases and potential therapeutic opportunities.Molecular biomedicine · 2026Review
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- Peli1, regulated by mCommunications biology · 2025Article
- Senescent Cells: An Emerging Therapeutic Target for Hemodialysis Fistula Maturation.Kidney360 · 2025Article
- Multifaceted roles of Meg3 in cellular senescence and atherosclerosis.Atherosclerosis · 2024Article
- Senescence induces fundamental changes in the secretome of mesenchymal stromal cells (MSCs): implications for the therapeutic use of MSCs and their derivates.Frontiers in bioengineering and biotechnology · 2023Review
- Roles of Protein Post-Translational Modifications During Adipocyte Senescence.International journal of biological sciences · 2023Review
- The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities.Cell & bioscience · 2022Review
- Irisin Suppresses Nicotine-Mediated Atherosclerosis by Attenuating Endothelial Cell Migration, Proliferation, Cell Cycle Arrest, and Cell Senescence.Frontiers in cardiovascular medicine · 2022Article
- MRKNs: Gene, Functions, and Role in Disease and Infection.Frontiers in oncology · 2022Review
- Construction of a circRNA-miRNA-mRNA Regulatory Network for Coronary Artery Disease by Bioinformatics Analysis.Cardiology research and practice · 2022Article
- Disturbed flow-induced FAK K152 SUMOylation initiates the formation of pro-inflammation positive feedback loop by inducing reactive oxygen species production in endothelial cells.Free radical biology & medicine · 2021Article
- Nuclear envelope tethering inhibits the formation of ALT-associated PML bodies in ALT cells.Aging · 2021Article
- Vascular Endothelial Senescence: Pathobiological Insights, Emerging Long Noncoding RNA Targets, Challenges and Therapeutic Opportunities.Frontiers in physiology · 2021Review
- Involvement of Senescence and Mitochondrial Fission in Endothelial Cell Pro-Inflammatory Phenotype Induced by Angiotensin II.International journal of molecular sciences · 2020Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDisturbed flow (d-flow)-induced senescence and activation of endothelial cells (ECs) have been suggested to have critical roles in promoting atherosclerosis. Telomeric repeat-binding factor 2 (TERF2)-interacting protein (TERF2IP), a member of the shelterin complex at the telomere, regulates the senescence-associated secretory phenotype (SASP), in which EC activation and senescence are engendered simultaneously by p90RSK-induced phosphorylation of TERF2IP S205 and subsequent nuclear export of the TERF2IP-TERF2 complex. In this study, we investigated TERF2IP-dependent gene expression and its role in regulating d-flow-induced SASP.
methodsA principal component analysis and hierarchical clustering were used to identify genes whose expression is regulated by TERF2IP in ECs under d-flow conditions. Senescence was determined by reduced telomere length, increased p53 and p21 expression, and increased apoptosis; EC activation was detected by NF-κB activation and the expression of adhesion molecules. The involvement of TERF2IP S205 phosphorylation in d-flow-induced SASP was assessed by depletion of TERF2IP and mutation of the phosphorylation site.
resultsOur unbiased transcriptome analysis showed that TERF2IP caused alteration in the expression of a distinct set of genes, including rapamycin-insensitive companion of mTOR (RICTOR) and makorin-1 (MKRN1) ubiquitin E3 ligase, under d-flow conditions. In particular, both depletion of TERF2IP and overexpression of the TERF2IP S205A phosphorylation site mutant in ECs increased the d-flow and p90RSK-induced MKRN1 expression and subsequently inhibited apoptosis, telomere shortening, and NF-κB activation in ECs via suppression of p53, p21, and telomerase (TERT) induction.
conclusionsMKRN1 and RICTOR belong to a distinct reciprocal gene set that is both negatively and positively regulated by p90RSK. TERF2IP S205 phosphorylation, a downstream event of p90RSK activation, uniquely inhibits MKRN1 expression and contributes to EC activation and senescence, which are key events for atherogenesis.
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