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  • Open Access

    REVIEW

    The Yin–Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease

    Douglas M. Ruden*

    BIOCELL, Vol.50, No.1, 2026, DOI:10.32604/biocell.2025.072273 - 23 January 2026

    Abstract Stem cell fate decisions are increasingly understood through the dynamic interplay of two fundamental stress-adaptive programs: the integrated stress response (ISR) and the senescence-associated secretory phenotype (SASP). These pathways act as a Yin–Yang system, balancing beneficial and detrimental outcomes across development, tissue homeostasis, and disease. On the yin (protective) side, transient ISR activation and acute SASP signaling foster adaptation, embryonic patterning, wound healing, and regeneration. On the yang (maladaptive) side, chronic ISR signaling and unresolved SASP output drive stem cell exhaustion, fibrosis, inflammation, and tumorigenesis. This duality highlights their roles as both guardians and disruptors More > Graphic Abstract

    The Yin–Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease

  • Open Access

    ARTICLE

    Overexpression of miR-1283 Inhibits Cell Proliferation and Invasion of Glioma Cells by Targeting ATF4

    Hao Chen, Yi Zhang, Hai Su, Hui Shi, Qijiang Xiong, Zulu Su

    Oncology Research, Vol.27, No.3, pp. 325-334, 2019, DOI:10.3727/096504018X15251282086836

    Abstract It is well known that activating transcription factor 4 (ATF4) expression is closely associated with progression of many cancers. We found that miR-1283 could directly target ATF4. However, the precise mechanisms of miR-1283 in glioma have not been well clarified. Our study aimed to explore the interaction between ATF4 and miR-1283 in glioma. In this study, we found that the level of miR-1283 was dramatically decreased in glioma tissues and cell lines, the expression of ATF4 was significantly increased, and the low level of miR-1283 was closely associated with high expression of ATF4 in glioma More >

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