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Diabetes is a metabolic disease characterized by hyperglycemia. Over 90% of patients with diabetes have type 2 diabetes. Pancreatic β-cells are endocrine cells that produce and secrete insulin, an essential endocrine hormone that regulates blood glucose levels. Deficits in β-cell function and mass play key roles in the onset and progression of type 2 diabetes. Apoptosis has been considered as the main contributor of β-cell dysfunction and decrease in β-cell mass for a long time. However, recent studies suggest that β-cell failure occurs mainly due to increased β-cell dedifferentiation rather than limited β-cell proliferation or increased β-cell death. In this review, we summarize the current advances in the understanding of the pancreatic β-cell dedifferentiation process including potential mechanisms. A better understanding of β-cell dedifferentiation process will help to identify novel therapeutic targets to prevent and/or reverse β-cell loss in type 2 diabetes.
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http://dx.doi.org/10.3390/nu13051593 | DOI Listing |
Cureus
August 2025
Department of Surgery, Ayub Medical College, Abbottabad, PAK.
This report presents the case of a 62-year-old male who presented with a two-month history of right flank pain and decreased appetite. Clinical evaluation revealed a palpable, non-tender mass in the right flank, while laboratory tests demonstrated mild anemia (hemoglobin 9.3 g/dL) with otherwise normal renal function.
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Intrinsic genetic alterations and dynamic transcriptional changes contribute to the heterogeneity of solid tumors. Lung adenocarcinoma (LUAD) is characterized by its significant histological, cellular and molecular heterogeneity. The present study aimed to study the spatial transcriptomics of primary LUAD with initial hopes to decipher molecular characteristics of subtype transitions in LUAD progression, offering new insights for novel therapeutic strategies.
View Article and Find Full Text PDFBiochim Biophys Acta Rev Cancer
September 2025
Institute of Cancer Therapeutics, Faculty of Life Sciences, University of Bradford, Bradford, United Kingdom. Electronic address:
Cancer stem cells (CSCs) are central to tumour initiation, progression, and relapse, yet their dynamic and adaptive nature hampers therapeutic targeting. Once viewed as a fixed subpopulation, CSCs are now recognised as a fluid functional state that tumour cells can enter or exit, driven by intrinsic programs, epigenetic reprogramming, and microenvironmental cues. This plasticity complicates identification due to inconsistent marker expression and enables resistance, dormancy, and metastasis.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Otolaryngology-Head and Neck Surgery, Nihon University School of Medicine, Tokyo, Japan.
Glottic insufficiency results from impaired vocal fold contact, leading to a gap between the folds and manifesting as hoarseness and respiratory difficulties. Vocal folds injection is a commonly utilized therapeutic approach to rectify this gap by augmenting vocal folds volume; however, the optimal injectable material remains undetermined. Dedifferentiated fat cells (DFATs), derived from mature adipocytes, exhibit robust proliferative capacity and multipotency, establishing them as potential candidates for treating glottic insufficiency.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Radiation Oncology, Stanford University, Stanford, CA 94305.
Reduced mitochondrial quality and quantity in tumors is associated with dedifferentiation and increased malignancy. However, it remains unclear how to restore mitochondrial quantity and quality in tumors and whether mitochondrial restoration can drive tumor differentiation. Our study shows that restoring mitochondrial function using retinoic acid (RA) to boost mitochondrial biogenesis and a mitochondrial uncoupler to enhance respiration synergistically drives neuroblastoma differentiation and inhibits proliferation.
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