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Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the developed world. While great advances have been made in the treatment of the neovascular ("wet") form of the disease, there is still a significant need for therapies that prevent the vision loss associated with the advanced forms of dry, atrophic AMD. In this atrophic form, retinal pigment epithelial (RPE) and photoreceptor cell death is the ultimate cause of vision loss. In this review, we summarize the cell death pathways and their relation to RPE and retinal cell death in AMD. We review the data that support targeting programmed cell death through inhibition of the Fas receptor as a novel approach to preserve these structures and that this effect results from inhibiting both canonical death pathway activation and reducing the associated inflammatory response. These data lay the groundwork for current clinical strategies targeting the Fas pathway in this devastating disease.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836408 | PMC |
http://dx.doi.org/10.3390/jcm11030592 | DOI Listing |
BMC Mol Cell Biol
September 2025
School of Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, UK.
Retinitis pigmentosa (RP) affects around 1 in 4000 individuals and represents approximately 25% of cases of vision loss in adults, through death of retinal rod and cone photoreceptor cells. It remains a largely untreatable disease, and research is needed to identify potential targets for therapy. Mutations in 94 different genes have been identified as causing RP, including AGBL5 which encodes the main deglutamylase that regulates and maintains functional levels of cilia tubulin glutamylation, which is essential to initiate ciliogenesis, maintain cilia stability and motility.
View Article and Find Full Text PDFSci China Life Sci
September 2025
MOE Key Laboratory of Bioinformatics and Center for Plant Biology, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Tomato brown rugose fruit virus (ToBRFV) overcomes all known tomato resistance genes, including the durable Tm-2, posing a serious threat to global tomato production. Here, we employed in vitro random mutagenesis to evolve the Tm-2 leucine-rich repeat (LRR) domain and screened ∼8,000 variants for gain-of-function mutants capable of recognizing the ToBRFV movement protein (MP) and triggering hypersensitive cell death. We identified five such mutants.
View Article and Find Full Text PDFNat Aging
September 2025
Aging Biomarker Consortium (ABC), Beijing, China.
The global surge in the population of people 60 years and older, including that in China, challenges healthcare systems with rising age-related diseases. To address this demographic change, the Aging Biomarker Consortium (ABC) has launched the X-Age Project to develop a comprehensive aging evaluation system tailored to the Chinese population. Our goal is to identify robust biomarkers and construct composite aging clocks that capture biological age, defined as an individual's physiological and molecular state, across diverse Chinese cohorts.
View Article and Find Full Text PDFBr J Cancer
September 2025
Institute of Life Sciences, Bhubaneswar, Odisha, India.
Background: Docetaxel is the most common chemotherapy regimen for several neoplasms, including advanced OSCC (Oral Squamous Cell Carcinoma). Unfortunately, chemoresistance leads to relapse and adverse disease outcomes.
Methods: We performed CRISPR-based kinome screening to identify potential players of Docetaxel resistance.
Cell 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.
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