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Many different types of programmed cell death (PCD) have been identified, including apoptosis and necroptosis. Apoptosis is a type of cell death that is controlled by various genes. It is in charge of eliminating aberrant cells such as cancer cells, replenishing normal cells, and molding the body as it develops. Necroptosis is a type of programmed cell death that combines necrosis and apoptosis. In other words, it takes on a necrotic appearance, although cells die in a controlled manner. Various investigations of these two pathways have revealed that caspase-8, receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3 are crucial proteins in charge of the switching between these two pathways, resulting in the activation or inhibition of necroptosis. In this review, we have summarized the key proteins between apoptosis and necroptosis.
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http://dx.doi.org/10.1155/2021/3420168 | DOI Listing |
Med Int (Lond)
August 2025
Hunan Provincial Hospital of Integrated Traditional Chinese and Western Medicine (The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine), Changsha, Hunan 410060, P.R. China.
S-glutathionylation (SSG), a redox-sensitive post-translational modification mediated by glutathione, regulates protein structure and function through reversible disulfide bond formation at cysteine residues. Glutaredoxins (GRXs), pivotal antioxidant enzymes, catalyze SSG dynamics to maintain thiol homeostasis. Recent advances in redox proteomics have revealed that SSG dysregulation is intricately linked to neurodegenerative, cardiovascular, pulmonary and malignant diseases.
View Article and Find Full Text PDFCell Death Differ
September 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by inflammatory demyelination and progressive neurodegeneration. Although current disease-modifying therapies modulate peripheral autoimmune responses, they are insufficient to fully prevent tissue specific neuroinflammation and long-term neuronal and oligodendrocyte loss. Growing evidence implicates various regulated cell death (RCD) pathways, including apoptosis, necroptosis, pyroptosis, and ferroptosis, not only as downstream consequences of chronic inflammation, but also as active drivers of demyelination, axonal injury, and glial dysfunction in MS.
View Article and Find Full Text PDFJ Ethnopharmacol
September 2025
Institute of Respiratory Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. Electronic address:
Ethnopharmacological Relevance: The high mortality rate associated with severe influenza partly results from delayed initiation of antiviral therapy and subsequent cytokine storms. Jiuwei Qianghuo Decoction combined with Zhuye Shigao Decoction (JZF) has been clinically prescribed to prevent the progression to a more severe illness in influenza treatment. However, the precise mode of action and active components have not yet been elucidated.
View Article and Find Full Text PDFInfect Immun
September 2025
School of Veterinary Medicine and Biomedical Sciences, University of Nebraska, Lincoln, Nebraska, USA.
Cell death mechanisms play a fundamental role in mycobacterial pathogenesis. We critically reviewed 94 research manuscripts, 44 review articles, and 4 book chapters to analyze important discoveries, background literature, and potential shortcomings in the field. The focus of this review is the pathogen (Mtb) and other Mtb and complex microorganisms.
View Article and Find Full Text PDFApoptosis
September 2025
School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
A defining hallmark of malignant tumours lies in their pronounced resistance to programmed cell death mechanisms. This intrinsic resilience enables cancer cells to circumvent physiological clearance, thereby sustaining unchecked proliferation and survival. Emerging research has revealed that metabolic dysregulation can precipitate a distinctive form of programmed cell death, termed metabolism-linked regulated cell death (RCD), establishing it as a novel paradigm of cellular self-elimination.
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