Trends in Pharmacological Sciences, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Trends in Pharmacological Sciences, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Experimental Hematology, Год журнала: 2025, Номер unknown, С. 104711 - 104711
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
2Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)
Опубликована: Март 7, 2025
Redox signaling acts as a critical mediator in the dynamic interactions between organisms and their external environment, profoundly influencing both onset progression of various diseases. Under physiological conditions, oxidative free radicals generated by mitochondrial respiratory chain, endoplasmic reticulum, NADPH oxidases can be effectively neutralized NRF2-mediated antioxidant responses. These responses elevate synthesis superoxide dismutase (SOD), catalase, well key molecules like nicotinamide adenine dinucleotide phosphate (NADPH) glutathione (GSH), thereby maintaining cellular redox homeostasis. Disruption this finely tuned equilibrium is closely linked to pathogenesis wide range Recent advances have broadened our understanding molecular mechanisms underpinning dysregulation, highlighting pivotal roles genomic instability, epigenetic modifications, protein degradation, metabolic reprogramming. findings provide foundation for exploring regulation mechanistic basis improving therapeutic strategies. While antioxidant-based therapies shown early promise conditions where stress plays primary pathological role, efficacy diseases characterized complex, multifactorial etiologies remains controversial. A deeper, context-specific signaling, particularly redox-sensitive proteins, designing targeted aimed at re-establishing balance. Emerging small molecule inhibitors that target specific cysteine residues proteins demonstrated promising preclinical outcomes, setting stage forthcoming clinical trials. In review, we summarize current intricate relationship disease also discuss how these insights leveraged optimize strategies practice.
Язык: Английский
Процитировано
1Pharmacological Research, Год журнала: 2025, Номер unknown, С. 107589 - 107589
Опубликована: Янв. 1, 2025
Bone marrow hematopoietic injury encompasses a range of pathological conditions that disrupt the normal function system, primarily through impaired production and differentiation bone cells. Key pathogenic mechanisms include aging, radiation damage, chemical induction, infection inflammation, cross-talk with non-hematopoietic diseases. These factors often lead to myelosuppression myeloid skewing. Furthermore, we explored potential application prospects natural products in treatment injury. Natural products, particularly those derived from Chinese herbal medicines other sources, have emerged as promising therapeutic options due their distinctive minimal side effects. A deeper understanding underlying could illuminate how exert effects, thereby optimizing strategies offering safer, more effective for patients. Future research should leverage emerging technologies further elucidate composition interactions within microenvironment, well specific pathways which modulate dysfunction.
Язык: Английский
Процитировано
0Current Opinion in Immunology, Год журнала: 2025, Номер 93, С. 102525 - 102525
Опубликована: Янв. 18, 2025
Язык: Английский
Процитировано
0Seminars in Cancer Biology, Год журнала: 2025, Номер 111, С. 1 - 15
Опубликована: Фев. 9, 2025
Язык: Английский
Процитировано
0Bone Research, Год журнала: 2025, Номер 13(1)
Опубликована: Март 3, 2025
Abstract Osteoporosis represents a prevalent and debilitating comorbidity in patients diagnosed with type 2 diabetes mellitus (T2DM), which is characterized by suppressed osteoblast function disrupted bone microarchitecture. In this study, we utilized male C57BL/6 J mice to investigate the role of SIRT3 T2DM. Decreased expression impaired mitochondrial quality control mechanism are observed both vitro vivo models Mechanistically, suppression results hyperacetylation FOXO3, hindering activation PINK1/PRKN mediated mitophagy pathway resulting accumulation dysfunctional mitochondria. Genetical overexpression or pharmacological restores deacetylation status thus facilitating ameliorating osteogenic impairment Collectively, our findings highlight fundamental regulatory control, crucial for maintaining homeostasis These insights not only enhance understanding molecular mechanisms underlying diabetic osteoporosis but also identify as promising therapeutic target osteoporosis.
Язык: Английский
Процитировано
0Nature Aging, Год журнала: 2025, Номер unknown
Опубликована: Март 6, 2025
Язык: Английский
Процитировано
0Food Hydrocolloids, Год журнала: 2024, Номер 160, С. 110848 - 110848
Опубликована: Ноя. 15, 2024
Язык: Английский
Процитировано
1Trends in Pharmacological Sciences, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
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