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Publications

Journal Article Review Epublish

PubMed: 40617807 DOI: 10.1038/s41419-025-07800-z

Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.

Cell Death Dis 16(1):495

Authors: Huan-Shao Huang, Lan Chen, Jia-Xin Chi, Shi-Ying Lai, Jiang Pi, Yi-Ming Shao, Jun-Fa Xu

Affiliations

  • Dongguan Key Laboratory of Pathogenesis and Experimental Diagnosis of Infectious Diseases, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China. Institute of Laboratory Medicine, School of Medical Technology, Guangdong Medical University, Dongguan, China. Songshan Lake Innovation Center of Medicine & Engineering, Guangdong Medical University, Dongguan, China.
  • Dongguan Key Laboratory of Pathogenesis and Experimental Diagnosis of Infectious Diseases, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China. Institute of Laboratory Medicine, School of Medical Technology, Guangdong Medical University, Dongguan, China.
  • Institute of Laboratory Medicine, School of Medical Technology, Guangdong Medical University, Dongguan, China.
  • Dongguan Key Laboratory of Pathogenesis and Experimental Diagnosis of Infectious Diseases, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China.
  • Dongguan Key Laboratory of Pathogenesis and Experimental Diagnosis of Infectious Diseases, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, China. Institute of Laboratory Medicine, School of Medical Technology, Guangdong Medical University, Dongguan, China. Songshan Lake Innovation Center of Medicine & Engineering, Guangdong Medical University, Dongguan, China.

Abstract

Pathogens exploit cellular stress responses to drive infection and evade immune responses, posing a persistent global health threat. Stress granules (SGs), dynamic mRNA hubs formed under stress, and regulated cell death (RCD) pathways collectively orchestrate host-pathogen dynamics. While SGs regulate mRNA translation to aid adaptation, RCD mechanisms-including apoptosis, pyroptosis, and necroptosis-eliminate infected cells to curb pathogen spread. However, pathogens subvert these systems through immune evasion strategies, such as disrupting SGs assembly or hijacking cell death signaling, to enhance replication and persistence. This review integrates molecular insights into SGs biogenesis and RCD regulation, dissecting their bidirectional interplay during infection. We highlight pathogen-specific tactics, such as viral proteases cleaving G3BP1 or bacterial effectors halting translation, to manipulate SGs dynamics and cell death pathways. Furthermore, we explore therapeutic opportunities targeting SGs assembly (e.g., eIF2α phosphorylation modulators, G3BP1 inhibitors) and RCD modulation (e.g., PANoptosis suppression, ferroptosis inducers) to restore host defense and mitigate immunopathology. By bridging molecular mechanisms with clinical applications, this analysis charts a course toward precision therapies leveraging the SGs-RCD axis to combat infectious diseases.

MeSH

Cells, Stress, Physiological, Therapeutics, Communicable Diseases, Cell Death, Infections