Bid Protein: A Participant in the Apoptotic Network with Roles in Viral Infections

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2385 - 2385

Published: March 7, 2025

The BH3-interacting domain death agonist (Bid), a proapoptotic signaling molecule of the B-cell lymphoma 2 (Bcl-2) family, is key regulator mitochondrial outer membrane (MOM) permeability. Uniquely positioned at intersection extrinsic and intrinsic apoptosis pathways, Bid links receptor to mitochondria-dependent cascade can also be activated by endoplasmic reticulum (ER) stress. In its active forms, cleaved (cBid) truncated (tBid), it disrupts MOM integrity via Bax/Bak-dependent independent mechanisms. Apoptosis plays dual role in viral infections, either promoting or counteracting propagation. Consequently, viruses modulate favor their replication. deregulation activity contributes oncogenic transformation, inflammation, immunosuppression, neurotoxicity, pathogen propagation during various infections. this work, we explore Bid’s structure, function, activation processes, targeting. We describe induction involvement infections with multiple viruses. Additionally, discuss therapeutic potential antiviral strategies. Understanding pathways offers valuable insights into host–virus interactions pathogenesis This knowledge may facilitate development novel approaches combat virus-associated diseases effectively.

Language: Английский

Peste des petits ruminants virus (PPRV) induces ferroptosis via LONP1-mediated mitochondrial GPX4 degradation in cell culture

Journal of Virology, Journal Year: 2025, Volume and Issue: unknown

Published: April 8, 2025

ABSTRACT Peste des petits ruminants virus (PPRV) is an important pathogen that seriously affects the productivity of small worldwide. Ferroptosis a programmed cell death characterized by iron-dependent lipid peroxidation and accumulation reactive oxygen species (ROS). Emerging evidence has demonstrated mitochondria play diverse roles in process ferroptosis, but interaction between ferroptosis during infection remains largely unknown. Here, we demonstrate PPRV induces including Fe 2+ overload, peroxidation, shrinkage mitochondria. Importantly, crucial role PPRV-induced decreased mitochondrial GPX4 Mechanistically, downregulates Lon protease-1 (LONP1) expression, multifaceted enzyme essential for maintaining homeostasis function, which leads to degradation through Nrf2/Keap pathway ROS More importantly, tightly associated with inflammatory responses enhanced replication. Overall, this study first show LONP1-mediated involved infection. IMPORTANCE transient severe immunosuppression host, threatens both livestock endangered susceptible wildlife populations many countries. Despite extensive research, it unknown whether causes what mechanism regulation is. Our data provide direct relationship (LONP1)-mediated dysfunctional consequent induction pathogenesis. via mitochondria, replication levels. Taken together, our research provided new insight into understanding effect on pathogenesis revealed potential therapeutic target antiviral intervention.

Language: Английский

Unveiling ferroptosis: a new frontier in skin disease research

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 4, 2024

Ferroptosis, a form of regulated cell death distinct from apoptosis, necrosis, and autophagy, is increasingly recognized for its role in skin disease pathology. Characterized by iron accumulation lipid peroxidation, ferroptosis has been implicated the progression various conditions, including psoriasis, photosensitive dermatitis, melanoma. This review provides an in-depth analysis molecular mechanisms underlying compares cellular effects with other forms context health disease. We systematically examine five specific diseases, ichthyosis, polymorphous light eruption (PMLE), vitiligo, melanoma, detailing influence on pathogenesis progression. Moreover, we explore current clinical landscape ferroptosis-targeted therapies, discussing their potential managing treating diseases. Our aim to shed therapeutic modulating research practice.

Language: Английский