生化学および細胞生物学ジャーナル

オープンアクセス

当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い

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700 ジャーナル 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得

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Cell Death: Mechanisms, Implications, and Therapeutic Approaches

Gleeson J

Cell death is a fundamental biological process essential for development, tissue homeostasis, and the removal of damaged or unwanted cells. This abstract provides a concise overview of the diverse mechanisms of cell death, their physiological implications, and the therapeutic strategies targeting cell death pathways. The major forms of cell death include apoptosis, necrosis, autophagy, and programmed necrosis [1,. Apoptosis, often referred to as programmed cell death, plays a crucial role in embryogenesis, immune response, and the maintenance of tissue integrity. Necrosis, traditionally considered accidental cell death, is now recognized as a regulated process under specific conditions. Autophagy, a self-eating process, serves as a cellular recycling mechanism and is closely linked to cell survival and death decisions. Programmed necrosis, or necroptosis, represents a form of cell death with characteristics of both apoptosis and necrosis. Dysregulation of cell death processes is implicated in various pathological conditions, including cancer, neurodegenerative diseases, and autoimmune disorders. Understanding the intricate balance between cell survival and death is critical for developing targeted therapies. Small molecules, gene therapies, and immunotherapies are among the promising strategies aimed at modulating cell death for therapeutic purposes. This abstract highlights the importance of unraveling the molecular mechanisms governing cell death and underscores the potential of manipulating these pathways for clinical interventions. A comprehensive understanding of cell death is crucial not only for advancing basic science but also for developing innovative therapies that can selectively target diseased cells while preserving normal tissue homeostasis.

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