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Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models

ABSTRACT: Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models

PROVIDER: PRJNA956991 | ENA |

REPOSITORIES: ENA

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Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models

Project description:this work shows the safe reduction of the biological age of ex vivo human skins by a senomorphic peptide.

2023-04-20 | GSE230026 | GEO

Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models.

Project description: Not available

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Tomatidine is a senotherapeutic compound that improves cognitive function and reduces cellular senescence in aged mice

Project description:Cellular senescence contributes to aging and age-related dysfunction across multiple tissues, including the brain. Here, we identify tomatidine, an aglycone of tomatine naturally found in tomatoes, as a senotherapeutic agent. In vitro, tomatidine selectively suppressed SASP expression without affecting p16Ink4a or p21Cip1 levels in senescent human brain microvascular endothelial cells. In aged mice, dietary tomatidine reduced frailty and improved motor coordination and cognitive performance. These functional benefits were accompanied by a reduction in senescence markers (e.g., p16, p21, and telomere-associated DNA damage foci) in liver, skin, and hippocampal neurons, as well as decreased neuroinflammation and microglial activation. Tomatidine also reduced senescence in brain endothelial cells and increased the expression of tight junction–associated proteins. Together, these findings suggest that tomatidine is as a promising senotherapeutic with the potential to preserve cognitive and vascular function during aging. As a naturally occurring compound with oral bioavailability and a favorable safety profile, tomatidine holds strong translational promise for future therapeutic development.

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Tomatidine is a senotherapeutic compound that improves cognitive function and reduces cellular senescence in aged mice

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LsCLE12 peptide delays senescence in lettuce and prolongs postharvest life of roses

Project description:The widespread use of chemical inputs in agriculture has raised concern over their long-term environmental and health impacts, driving demand for sustainable, natural product-based alternatives. Peptide-hormone signaling interactions, particularly those regulating senescence, are promising targets for developing such alternatives to advance postharvest technologies. However, most current insights stem from model species, limiting their translation to crops and ornamental plants. This study identifies the CLAVATA3/EMBRYO-SURROUNDING REGION-related (CLE) family CLE12 peptide (CLE12p) in Lactuca sativa as a peptide that shows potential for postharvest management of crops and ornamental flowers. CLE12p interacts with salt (NaCl), abscisic acid (ABA) and ethylene pathways, influencing lettuce development and morphology. Notably, CLE12p induced stomatal closure in a similar manner to that of ABA, suggesting overlapping signalling pathways. Transcriptomic analyses revealed how CLE12p modulates immune and defence responses, fluid transport, and leaf senescence, indicating a broader role in leaf senescence regulation similar to that of ethylene. Functionally, CLE12p delayed senescence in lettuce by preserving leaf greenness and water content following dark treatment and harvest. Additionally, CLE12p extended the longevity of cut roses by maintaining fresh weight and water content. These findings demonstrate the practical potential of CLE peptides in non-model species and support their application as natural tools for extending postharvest shelf life in crops and ornamental plants, paving the way for further exploration of their role in agricultural biotechnology.

2025-11-18 | GSE299676 | GEO

Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes

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FXR Agonism with Bile Acid Mimetic Reduces Pre-Clinical Triple-Negative Breast Cancer Burden

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LsCLE12 peptide delays senescence in lettuce and prolongs postharvest life of roses

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PRDM16 reduces cellular senescence by upregulating GSTM1

Project description:Cellular senescence is a hallmark of aging and the accumulation of senescent cells (SnCs) accelerates the aging process, contributing to aging-related organ disorders. The PRDF1 and RIZ1 homology domain (PRDM) protein exhibits robust transcriptional regulatory activities and governs a wide range of biological processes. However, its roles in cellular senescence remain unclear. Here, we demonstrated that PRDM16, a member of the PRDM protein family, decreased significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributed to cellular senescence in various organs, including the kidneys, heart, lungs, hippocampus, stomach, and gut, leading to accelerated aging-related organ injury. Furthermore, tubular-specific Prdm16 deletion aggravated irradiation-induced kidney aging and aging-related kidney diseases in irradiated mice subjected to ischemia-reperfusion surgery. Exogenous PRDM16 gene delivery by lentivirus effectively attenuated cellular senescence in vitro and in vivo. Mechanistically, PRDM16 improved glutathione metabolism and inhibited oxidative DNA damage, which is a driving force of senescence. Specifically, PRDM16 upregulated the transcription of glutathione S-transferase mu 1 (GSTM1) by binding to its promoter region. Transfection with GSTM1 reversed PRDM16 deficiency-induced cellular senescence and kidney aging. Collectively, our results provide a potential target for the investigation of anti-aging therapies.

2025-09-02 | GSE307024 | GEO

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