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decreases. Distinct from the features of necrosis, autophagy, and apoptosis, ferroptosis could result in compromised plasma membrane integrity, mild chromatin condensation, cytoplasm and cytoplasmic organelles swelling, increased mitochondrial membrane
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secreted from pancreatic cells. PANDER has been shown to influence glycolipid metabolism by inducing apoptosis in pancreatic β cells, inhibiting insulin secretion ( 6 , 7 , 8 ), promoting hepatic glucose production, and stimulating lipogenesis ( 9 , 10
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apoptosis of cardiomyocytes ( 29 ). In addition, SDF-1 can aggravate cardiac remodeling and worsen cardiac function by enhancing the proliferation of cardiac fibroblasts and collagen production ( 30 ). Correspondingly, plasma SDF-1 levels can serve as a
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fibrosis in T2DM mice. Studies have found that with the development of T2DM, renal tissue will appear obvious fibrosis in the later stage, while hyperglycemia leads to internal environmental inflammation, oxidative stress and apoptosis, which increases the
Department of Endocrinology, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
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and decreased insulin biosynthesis and secretion) ( 1 , 2 ). Of these factors, ER and oxidative stress are well known to affect receptor‐signal transduction, gene expression, and ion channel transport and induce cell apoptosis and death ( 3 ). The
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neuropathy ( 34 , 35 , 36 ). NLRP3 induces cellular scorching, a specific form of inflammation-driven apoptosis ( 37 ). Activation of NLRP3 is observed in mouse models of diabetic nephropathy and in podocytes after angiotensin-II-aldosterone stimulation
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apoptosis), autophagy, bone remodeling, atherosclerosis, tumor metastasis, as well as roles in inflammation and cerebral amyloid angiopathy ( 10 , 11 ). Actually, CysC is a disease-associated protein, and alteration in CysC levels may suggest important
Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China
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Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China
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Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China
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Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China
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Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China
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. Diabetes 2008 57 696 – 705 . ( https://doi.org/10.2337/db07-1098 ) 44 He C Zhu H Li H Zou MH Xie Z . Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes
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Institute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
PhD Program in Toxicology, Kaohsiung Medical University, Kaohsiung, Taiwan
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Faculty of Medicine, National Yang Ming Chiao Tung University School of Medicine, Taipei, Taiwan
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a perpetrator of oxidative stress ( 6 ). The in vitro and in vivo studies have identified that acrolein-induced oxidative damage can lead to mitochondrial and DNA dysfunction and exacerbate apoptosis ( 20 ). Acrolein also inhibits antioxidant
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reactive oxygen species, resulting in the apoptosis of T cells, inhibition of T cell proliferation, as well as expansion of T-regulatory cells (Tregs) ( 4 , 5 ). Tregs play a critical role in maintaining immune homeostasis and preventing the development