Autophagy and Its Association with Macrophages in Clonal Hematopoiesis Leading to Atherosclerosis DOI Open Access
Shuanhu Li, Xin Zhou,

Qinchun Duan

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3252 - 3252

Published: April 1, 2025

Atherosclerosis, a chronic inflammatory disease characterized by lipid accumulation and immune cell infiltration, is linked to plaque formation cardiovascular events. While traditionally associated with metabolism endothelial dysfunction, recent research highlights the roles of autophagy clonal hematopoiesis (CH) in its pathogenesis. Autophagy, cellular process crucial for degrading damaged components, regulates macrophage homeostasis inflammation, both which are pivotal atherosclerosis. In macrophages, influences metabolism, cytokine regulation, oxidative stress, helping prevent instability. Defective exacerbates impairs cholesterol efflux, accelerates progression. Additionally, autophagic processes cells smooth muscle further contribute atherosclerotic pathology. Recent studies also emphasize interplay between CH, wherein somatic mutations genes like TET2, JAK2, DNMT3A drive expansion enhance responses plaques. These modify function, intensifying environment accelerating Chaperone-mediated (CMA), selective form autophagy, plays critical role regulating inflammation pro-inflammatory cytokines oxidized low-density lipoprotein (ox-LDL). Impaired CMA activity leads these substrates, activating NLRP3 inflammasome worsening inflammation. Preclinical suggest that pharmacologically may mitigate atherosclerosis animal models, reduced instability increases This review importance regulation focusing on formation, contributions CH. Building upon current advances, we propose hypothesis programmed death, intrinsic axis modulates fundamental functions playing complex development Understanding mechanisms offers potential therapeutic strategies targeting reduce burden disease.

Language: Английский

Safety, Efficacy and Bio-Distribution Analysis of Exosomes Derived From Human Umbilical Cord Mesenchymal Stem Cells for Effective Treatment of Bronchopulmonary Dysplasia by Intranasal Administration in Mice Model DOI Creative Commons
Wanting Xu,

Xiaolin Jieda,

Yue Wu

et al.

International Journal of Nanomedicine, Journal Year: 2025, Volume and Issue: Volume 20, P. 2521 - 2553

Published: Feb. 1, 2025

Exosomes (Exos) derived from human umbilical cord mesenchymal stem cells (hUC-MSCs) hold great potential for treating bronchopulmonary dysplasia (BPD); however, safety concerns and effects of intranasal administration remain unexplored. This study aimed to explore the hUC-MSCs Exos investigate efficacy bio-distribution repeated in neonatal BPD models. Characteristics were analyzed. A subcutaneous tumor formation assay using a single dose or was conducted Crl:NU-Foxn1nu mice. Vital signs, biochemical indices, pathological alterations, 18F-FDG microPET/CT analysis examined. Pulmonary pathology, three-dimensional reconstructions, ultrastructural structures, vivo ex imaging analyses, enzyme-linked immunoassay assays, reverse transcription-quantitative polymerase chain reaction analyses lung tissues all documented following administration. satisfied specifications. mice did not exhibit overt toxicity carcinogenicity after 60 days observation. Repeated effectively alleviated injuries, restored pulmonary ventilation reconstruction, recovered endothelial cell layer integrity analysis. steadily accumulated postnatal day 1 14. also interrupted epithelial-mesenchymal transition inflammation reactions As nanoscale, non-cellular therapy, an effective, noninvasive treatment BPD. approach free toxic, tumorigenic risks repaired alveolar damage while interrupting with

Language: Английский

Citations

0
Autophagy and Its Association with Macrophages in Clonal Hematopoiesis Leading to Atherosclerosis DOI Open Access
Shuanhu Li, Xin Zhou,

Qinchun Duan

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3252 - 3252

Published: April 1, 2025

Atherosclerosis, a chronic inflammatory disease characterized by lipid accumulation and immune cell infiltration, is linked to plaque formation cardiovascular events. While traditionally associated with metabolism endothelial dysfunction, recent research highlights the roles of autophagy clonal hematopoiesis (CH) in its pathogenesis. Autophagy, cellular process crucial for degrading damaged components, regulates macrophage homeostasis inflammation, both which are pivotal atherosclerosis. In macrophages, influences metabolism, cytokine regulation, oxidative stress, helping prevent instability. Defective exacerbates impairs cholesterol efflux, accelerates progression. Additionally, autophagic processes cells smooth muscle further contribute atherosclerotic pathology. Recent studies also emphasize interplay between CH, wherein somatic mutations genes like TET2, JAK2, DNMT3A drive expansion enhance responses plaques. These modify function, intensifying environment accelerating Chaperone-mediated (CMA), selective form autophagy, plays critical role regulating inflammation pro-inflammatory cytokines oxidized low-density lipoprotein (ox-LDL). Impaired CMA activity leads these substrates, activating NLRP3 inflammasome worsening inflammation. Preclinical suggest that pharmacologically may mitigate atherosclerosis animal models, reduced instability increases This review importance regulation focusing on formation, contributions CH. Building upon current advances, we propose hypothesis programmed death, intrinsic axis modulates fundamental functions playing complex development Understanding mechanisms offers potential therapeutic strategies targeting reduce burden disease.

Language: Английский

Citations

0