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Biomedicine & Pharmacotherapy =... Dec 2023Diabetes mellitus is a metabolic disease caused by disorders of insulin secretion and utilization. Long-term hyperglycemia, insulin resistance, and disorders of glucose... (Review)
Review
Diabetes mellitus is a metabolic disease caused by disorders of insulin secretion and utilization. Long-term hyperglycemia, insulin resistance, and disorders of glucose and lipid metabolism cause vascular endothelial cell damage. Endothelial dysfunction is a key feature of diabetic vascular complications such as diabetic nephropathy, retinopathy, neuropathy, and atherosclerosis. Importantly, cell death is thought to be a key factor contributing to vascular endothelial injury. Morphologically, cell death can be divided into three forms: type I apoptosis, type II autophagy, and type III necrosis. According to the difference in function, cell death can be divided into accidental cell death (ACD) and regulated cell death (RCD). RCD is a controlled process involving numerous proteins and precise signaling cascades. Multiple subroutines covered by RCD may be involved in diabetic endothelial dysfunction, including apoptosis, autophagy, necroptosis, pyroptosis, entosis, ferroptosis, ferroautophagy, parthanatos, netotic cell death, lysosome-dependent cell death, alkaliptosis, oxeiptosis, cuproptosis, and PANoptosis. This article briefly reviews the mechanism and significance of cell death associated with diabetic endothelial dysfunction, which will help deepen the understanding of diabetic endothelial cell death and provide new therapeutic ideas.
Topics: Humans; Cell Death; Diabetes Mellitus; Apoptosis; Necrosis; Regulated Cell Death
PubMed: 37918258
DOI: 10.1016/j.biopha.2023.115802 -
Nature Medicine Feb 2024Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA))...
Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau. Compelling genetic and biomarker evidence supports Aβ as the root cause of AD. We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt-Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds. This raised the possibility that c-hGH recipients who did not die from iCJD may eventually develop AD. Here we describe recipients who developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms. Although iatrogenic AD may be rare, and there is no suggestion that Aβ can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures. As propagating Aβ assemblies may exhibit structural diversity akin to conventional prions, it is possible that therapeutic strategies targeting disease-related assemblies may lead to selection of minor components and development of resistance.
Topics: Young Adult; Humans; Child; Alzheimer Disease; Growth Hormone; Amyloid beta-Peptides; Creutzfeldt-Jakob Syndrome; Cerebral Amyloid Angiopathy; Brain; Prions; Cadaver; Iatrogenic Disease; Biomarkers
PubMed: 38287166
DOI: 10.1038/s41591-023-02729-2 -
Scientific Reports Aug 2023Disulfidptosis is a newly discovered form of cell death. Not yet clearly classified as programmed cell death or accidental cell death. This study aimed to create a novel...
Disulfidptosis is a newly discovered form of cell death. Not yet clearly classified as programmed cell death or accidental cell death. This study aimed to create a novel disulfidptosis-related lncRNA index (DLI) that can be used to predict survival and chemotherapy drugs sensitivity in patients with cervical cancer. First of all, we found lncRNAs associated with disulfidptosis between cervical cancer tissues and normal tissues. By LASSO-Cox analysis, overlapping lncRNAs were then used to construct lncRNA index associated with disulfidptosis, which can be served to predict the prognosis of patients with CC, especially the chemotherapy drugs sensitivity. ROC curves and PCA based on DLI and clinical signatures were developed and demonstrated to have good predictive potential. In addition, differences in immune cell subset infiltration and differences in immune checkpoint expression between high-DLI and low-DLI groups were analyzed, and we investigated the relationship between the DLI and tumor mutation burden (TMB). In summary, we constructed a lncRNA prediction index associated with disulfidptosis. This has important clinical implications, including improving the predictive value of cervical cancer patients and providing a biomarker for cervical cancer guiding individualized treatment.
Topics: Humans; Female; RNA, Long Noncoding; Uterine Cervical Neoplasms; Prognosis; Apoptosis; Cell Death
PubMed: 37528124
DOI: 10.1038/s41598-023-39669-3