PANoptosis-Related Gene Biomarkers in Aortic Dissection

Archives of Biochemistry and Biophysics, Год журнала: 2025, Номер 768, С. 110385 - 110385

Опубликована: Март 12, 2025

Язык: Английский

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Costunolide: Targeting Endothelial Cell PANoptosis to Mitigate Lung Injury in Acute Pancreatitis Mice

Phytomedicine, Год журнала: 2025, Номер unknown, С. 156767 - 156767

Опубликована: Апрель 1, 2025

Язык: Английский

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TRIM56 Modulates YBX1 Degradation to Ameliorate ZBP1‐Mediated Neuronal PANoptosis in Spinal Cord Injury

Advanced Science, Год журнала: 2024, Номер unknown

Опубликована: Сен. 18, 2024

Abstract Spinal cord injury (SCI) is a severe to the central nervous system, and its treatment always major medical challenge. Proinflammatory cell death considered an important factor affecting neuroinflammation prognosis after injury. PANoptosis, newly discovered type of proinflammatory death, regulates activation executioner molecules apoptosis, pyroptosis necroptosis through PANoptosome, providing new target for therapeutic intervention SCI. However, role regulatory mechanism in SCI are not yet elucidated. Here, based on proteomic data, YBX1 expression significantly increased neurons Guided by RIP‐seq, subsequent experiments reveal that promotes ZBP1 stabilizing Zbp1 mRNA, thereby aggravating ZBP1‐mediated PANoptosis. Furthermore, E3 ubiquitin ligase TRIM56 identified as endogenous inhibitor via molecular docking IP/MS analysis. Mechanistically, bound promoted ubiquitination, accelerating degradation. Taken together, these findings novel function regulating PANoptosis pathogenesis verified functions promote ubiquitin‐proteasomal degradation YBX1, insights into strategies.

Язык: Английский

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Pathobiology of myocardial and cardiomyocyte injury in ischemic heart disease: Perspective from seventy years of cell injury research

Experimental and Molecular Pathology, Год журнала: 2024, Номер 140, С. 104944 - 104944

Опубликована: Ноя. 21, 2024

Язык: Английский

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BuyangHuanwu Decoction alleviates Endothelial Cell Apoptosis and Coronary Microvascular Dysfunction via Regulation of the MAPKK4/p38 Signaling Axis

International Journal of Medical Sciences, Год журнала: 2024, Номер 21(13), С. 2464 - 2479

Опубликована: Янв. 1, 2024

MAPKK4 has been implicated in the pathological mechanisms underlying myocardial and vascular injury, specifically influencing endothelial cell damage programmed death via subcellular pathways. Nevertheless, regulatory role of coronary microvascular injury following infarction remains unconfirmed, exploration targeted mitochondrial protective therapeutic agents unaddressed. In light this gap, we established a gene-modified mouse model ischemia-reperfusion employed Buyang Huanwu decoction (BYHW), traditional cardiovascular formula, to assess its efficacy treating post-ischemia-reperfusion. The study aimed elucidate mechanism by which BYHW mitigates induced through attenuation apoptosis. Experimental outcomes revealed that high-dose significantly ameliorated post-ischemia-reperfusion, restoring structural integrity microvasculature reducing inflammation oxidative stress. Contrarily, transgenic mice overexpressing MAPKK4, intervention failed attenuate To further investigate, simulated hypoxia/reoxygenation cells using MAPKK4-related cellular gene modification model. results indicated attenuates inflammatory enhances viability hypoxic stress, inhibiting apoptosis pathway. However, overexpression MAPKK4/p38 negated effects BYHW, showing no impact on stress under conditions. Molecular interaction studies confirmed active components Astragaloside IV Ligustrazine, interact with MAPKK4/P38 axis.

Язык: Английский

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In-situ Sprayed platelet-derived small extracellular vesicles for the skin flap survival by reducing PANoptosis

Biomaterials, Год журнала: 2024, Номер 316, С. 123001 - 123001

Опубликована: Дек. 6, 2024

Язык: Английский

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