Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: Nov. 28, 2024
Language: Английский
Seminars in Cancer Biology, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
2
Cytokine & Growth Factor Reviews, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
1
Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12
Published: Oct. 9, 2024
This article reviews the latest research progress on role of mitochondrial autophagy receptor FUN14 domain containing 1 (FUNDC1) in events and kidney disease. FUNDC1 is a protein located outer membrane mitochondria, which maintains function quality mitochondria by regulating autophagy, that is, selective degradation process mitochondria. The structural characteristics enable it to respond intracellular signal changes regulate activity through phosphorylation dephosphorylation. During phosphorylation, unc-51-like kinase (ULK1) promotes activation mitophagy phosphorylating Ser17 FUNDC1. In contrast, Src CK2 kinases inhibit interaction between LC3 Tyr18 Ser13, thereby inhibiting mitophagy. dephosphorylation, PGAM5 phosphatase enhances dephosphorylating activating BCL2L1 inhibits interacting with PGAM5, preventing dephosphorylation plays an important events, participating fission, maintaining homeostasis iron proteins matrix, mediating crosstalk endoplasmic reticulum lysosomes, have effects cell energy metabolism programmed death. aspect disease, abnormal closely related occurrence development many diseases. acute injury (AKI), cardiorenal syndrome (CRS), diabetic nephropathy (DN), chronic disease (CKD) ,renal fibrosis (RF) renal anemia, FUNDC1-mediated imbalance may be one key factors progression. Therefore, in-depth study regulatory mechanism great significance for understanding pathogenesis developing new treatment strategies.
Language: Английский
Citations
5
Trends in Cell Biology, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
Language: Английский
Citations
0
Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: March 26, 2025
Background Chronic heart failure (CHF) is one of the leading causes high mortality worldwide. It characterized by pathological hypertrophy and poses a major threat to human health. Aconiti Lateralis Radix Praeparata widely used in ancient China treat CHF. However, pathology obscured, necessitating further exploration. Methods Prospective targets were predicted network analysis. A transverse aortic constriction (TAC) mice model was subsequently constructed determine effects aqueous extract (AEA) on The echocardiography performed investigate cardiac function. Histopathological analysis tissue conducted assess myocardial fibrosis. Nontargeted metabolomics analyze serum metabolites. phosphorylation level PI3K AKT, downstream such as Bnip3, p62, Atg5, LC3II measured Western blotting. In vitro , norepinephrine (NE) stimulate hypertrophy. Parameters reactive oxygen species levels, mitochondrial membrane potential, ATP concentration, CK/MB content detected H9c2 cells. Results AEA significantly alleviated Network indicated participation AKT CHF, modulated Praeparata. vivo administration effectively ameliorated performance, evidenced elevation ejection fraction. displayed diminishment collagen fiber. Metabolomics showed that several metabolites tetrahydroxycorticosterone, decylubiquinone taurocholic acid increased TAC serum. Additionally, levels expression Drp1, Opa1, Atg5 altered group. NE stimulation cell surface area deteriorated functions partially reversed results, mechanism associated with mitophagy. Conclusion This study revealed improved function via PI3K/AKT/Bnip3 pathway.
Language: Английский
Citations
0
Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: May 19, 2025
Abstract Fibrotic skin diseases are characterized by excessive fibroblast proliferation and pathological extracellular matrix deposition. As a pivotal coenzyme in cellular energetics, NAD homeostasis perturbation is implicated fibrosis. Multiple studies have demonstrated the therapeutic potential of mesenchymal stem cells (MSCs) against cutaneous fibrosis, while specific mechanism remains elusive. Herein, this work finds that although almost all MSCs undergo situ apoptosis within 24 h post‐subcutaneous administration, MSC‐derived apoptotic bodies (ABs) mediated potent anti‐fibrotic effects. Mechanistically, ABs can restore mitochondrial through NAMPT transfer, FOXO1 deacetylation enhancement, PINK1/PARKIN‐dependent mitophagy activation. To achieve penetration into hard fibrotic skin, permeable (pABs) constructed via metabolic glycoengineering copper‐free click chemistry techniques. In both keloid xenograft scleroderma murine models, pABs significantly penetrate collagen reduce summary, research establishes highly promising strategy for reversing fibrosis with matrix.
Language: Английский
Citations
0
Biology Direct, Journal Year: 2025, Volume and Issue: 20(1)
Published: May 26, 2025
Sepsis is a life-threatening condition with limited therapeutic options, characterized as excessive systemic inflammation and multiple organ failure. Macrophages play critical roles in sepsis pathogenesis. Although numerous studies support the role of Notch signaling most inflammatory diseases, function Notch1 macrophages activation its underlying molecular mechanism during has not been fully elucidated. We evaluated expression lipopolysaccharide (LPS)-induced model septic cardiac dysfunction. Using macrophage-specific knockout mice (NOTCH1ΔMyelo) conjunction AAV-F4/80-mediated NICD1 overexpression, we investigated impact on injury. LPS-stimulated bone marrow-derived (BMDMs) were analyzed by flow cytometry ELISA to assess mitochondrial damage inflammasome activation. Mitophagy flux related protein levels quantified, mitophagy inhibitor was applied further delineate Notch1's vivo role. Downstream targets identified validated via ChIP-qPCR luciferase reporter assays. Intraperitoneal injection LPS markedly impaired function, increased macrophage infiltration, elevated compared PBS-treated controls. inversely correlated performance LPS-treated mice. Notably, deletion significantly improved whereas overexpression worsened LPS-induced NOTCH1ΔMyelo showed reduced diminished NLRP3-dependent caspase-1. Moreover, induced mitophagy, an effect that enhanced knockout. Mechanistically, ChIP-seq qPCR analyses revealed upregulates Mst1 transcription. Furthermore, counteracted Notch1-deficient macrophages, resulting reactive oxygen species production, cytokine secretion, caspase-1 prolonged stimulation. Our study uncovers novel for exacerbating dysfunction suppressing macrophages. These findings suggest targeting may offer promising strategy mitigate sepsis-induced restoring proper mitophagy.
Language: Английский
Citations
0
Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: unknown
Published: June 17, 2024
Language: Английский
Citations
2
Biosensors and Bioelectronics, Journal Year: 2024, Volume and Issue: 270, P. 116954 - 116954
Published: Nov. 17, 2024
Language: Английский
Citations
2
Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: Nov. 28, 2024
Language: Английский
Citations
1