
Neuropharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 110439 - 110439
Published: March 1, 2025
Language: Английский
Neuropharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 110439 - 110439
Published: March 1, 2025
Language: Английский
Microchemical Journal, Journal Year: 2025, Volume and Issue: unknown, P. 112801 - 112801
Published: Jan. 1, 2025
Language: Английский
Citations
0Breast Cancer Basic and Clinical Research, Journal Year: 2025, Volume and Issue: 19
Published: Jan. 1, 2025
Background: Breast cancer is the most common malignancy in women and leading cause of cancer-related death. Although early-stage patients are cured, 20% to 30% develop metastases, significantly reducing survival rates. Recent research highlights role iron progression, although its full impact on breast metastasis not yet fully understood. Objectives: The aim this study investigate association between plasma levels at diagnosis risk developing metastatic disease. Design: Retrospective single-center study. Methods: Patients with stage I III cancer, diagnosed 2007 2017, serum iron, transferrin saturation, ferritin values available within 1.5 months before or after were included. Cox proportional hazard models applied determine metastasis. Results: In total, 1113 included, 10% them developed distant over a median follow-up period 7 years. multivariable analysis adjusting for age, stage, subtype, saturation associated an increased For each increment baseline, there was 19% increase (hazard ratio [HR] = 1.19; 95% confidence interval [CI] [1.02-1.38]). Similarly, 10 µg/dL led 6% (HR 1.06; CI [1.01-1.12]). Ferritin found be 0.99; [0.98, 1.01]). There no significant site subtype when age stage. Conclusion: Elevated early disease but location metastases subtype. Further needed understand underlying mechanisms explore potential iron-targeted therapies.
Language: Английский
Citations
0Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: March 7, 2025
Proteotoxicity induced by misfolded or aggregated proteins causes progressive neuronal damage. The endoplasmic reticulum (ER) protein quality control (ERQC) pathways are responsible for mitigating the accumulation of these proteins, thus reducing proteotoxicity. Enhancing ERQC is a promising strategy treating neurodegenerative diseases. However, mechanisms governing initiation and degradation in neurons remain largely unknown vivo. In studying maturation proAVP mouse AVP neurons, this study discovers that autophagy ER-associated (ERAD) collaborate to maintain protect neuron survival against Autophagy deficiency leads late-onset diabetes insipidus. Mechanistically, selectively degrades mutant aggregates endogenous HRD1 SEL1L-HRD1 ERAD complex through FAM134B mediated ER-phagy. induction aggregation maintaining function under deficiency. Thus, form dual-protection system orchestrates prohormone endocrine survival, providing new insights complexity neuroendocrinology intrinsic mechanism diseases, with therapeutic potential folding
Language: Английский
Citations
0Published: March 1, 2025
Language: Английский
Citations
0Neuropharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 110439 - 110439
Published: March 1, 2025
Language: Английский
Citations
0