Neural Regeneration Research ›› 2025, Vol. 20 ›› Issue (3): 805-807.doi: 10.4103/NRR.NRR-D-24-00245

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Mitochondria–cGAS–STING axis is a potential therapeutic target for senescence-dependent inflammaging-associated neurodegeneration

José M. Izquierdo*   

  1. Centro de Biología Molecular Severo Ochoa (CBM), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain
  • Online:2025-03-15 Published:2024-06-26
  • Contact: José M. Izquierdo, PhD, jmizquierdo@cbm.csic.es.
  • Supported by:
    Research in the author’s laboratory is supported by the Ministry of Science and Innovation and the Spanish Research Agency through FEDER funds (PID2021-1261520B-100) (MICINN/AEI/FEDER, EU). CBM receives an institutional grant from the Fundación Ramón Areces, Spain.

Abstract: The word “senescence” comes from the Latin senescens, meaning “to begin to age”, and is characterized by a long-lasting but reversible block in proliferation, resulting from stress-induced cell cycle arrest of previously replication-competent cells. Many stress situations lead to senescence, including telomere shortening, genotoxic stress, oncogene- and oxidative-induced stress, and mitochondrial dysfunction (Mico et al., 2021). It is also characterized by a proinflammatory senescence-associated secretory phenotype (SASP) that potentiates chronic low-grade inflammation and inflammaging-associated dysfunction, resulting in loss of tissue function and health (Figure 1; Mico et al., 2021).