Melatonin Promotes Cerebral Angiogenesis in Ischemic Mice via BMP6/Smad1/5/9 Pathway DOI Creative Commons
Linlin Li,

Yujia Yuan,

Cong Zhang

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 25, 2025

Angiogenesis facilitates the reinstatement of blood supply to cerebral tissues after stroke by reconstructing vascular network, thereby rescuing penumbra region and restoring neural functions. Melatonin can modulate angiogenesis under a variety biological disease-related states, bone morphogenetic protein 6 (BMP6) targets regulators associated with angiogenesis. The specific functions melatonin BMP6 in following infarction, along potential intrinsic regulatory interactions between them, are currently unclear need further investigation. was given mice from 1st day through 28th post permanent distal middle artery occlusion (dMCAO). Our research revealed that enhanced neurological performance decreased size brain infarction. Additionally, it boosted circulation fostered area. Meanwhile, facilitated endothelial cells migration tube formation oxygen-glucose deprivation (OGD). promoted expression its downstream targets, Smad1/5/9, as well factors Vascular Endothelial Growth Factor (VEGF) Angiopoietin-1 (Ang1) vivo vitro, which counteracted or partially inhibited suppression expression. provides strong evidence promotes infarction BMP6/Smad1/5/9 signaling pathway, supporting restoration function.

Language: Английский

Much More than Nutrients: The Protective Effects of Nutraceuticals on the Blood–Brain Barrier in Diseases DOI Open Access

Anna E. Kocsis,

Nóra Kucsápszky,

Ana Raquel Santa-Maria

et al.

Nutrients, Journal Year: 2025, Volume and Issue: 17(5), P. 766 - 766

Published: Feb. 21, 2025

The dysfunction of the blood-brain barrier (BBB) is well described in several diseases, and considered a pathological factor many neurological disorders. This review summarizes most important groups natural compounds, including alkaloids, flavonoids, anthocyanidines, carotenoids, lipids, vitamins that were investigated for their potential protective effects on brain endothelium. penetration these compounds interaction with BBB efflux transporters solute carriers are discussed. cerebrovascular endothelium therapeutic target diseases. In preclinical studies modeling systemic central nervous system nutraceuticals exerted beneficial BBB. vivo, they decreased permeability, edema, astrocyte swelling, morphological changes vessel structure basal lamina. At level endothelial cells, increased cell survival apoptosis. From general functions, angiogenesis levels vasodilating agents demonstrated. elevated integrity by tightened intercellular junctions, expression activity transporters, such as pumps, carriers, metabolic enzymes, shown. Nutraceuticals enhanced antioxidative defense anti-inflammatory at signaling mediating stability activation WNT, PI3K-AKT, NRF2 pathways, inhibition MAPK, JNK, ERK, NF-κB pathways. represent valuable source new potentially molecules to treat diseases protecting

Language: Английский

Citations

1
Alzheimer’s, Parkinson’s, Frontotemporal Lobar Degeneration, and Amyotrophic Lateral Sclerosis Start in Pediatric Ages: Ultrafine Particulate Matter and Industrial Nanoparticles Are Key in the Early-Onset Neurodegeneration: Time to Invest in Preventive Medicine DOI Creative Commons
Lilian Calderón‐Garcidueñas, Angélica González-Maciel, Rafael Reynoso-Robles

et al.

Toxics, Journal Year: 2025, Volume and Issue: 13(3), P. 178 - 178

Published: Feb. 28, 2025

Billions of people are exposed to fine particulate matter (PM2.5) levels above the USEPA’s annual standard 9 μg/m3. Common emission sources anthropogenic, producing complex aerosolized toxins. Ultrafine (UFPM) and industrial nanoparticles (NPs) have major detrimental effects on brain, but USA does not measure UFPM a routine basis. This review focuses development progression common neurodegenerative diseases, as diagnosed through neuropathology, among young residents in Metropolitan Mexico City (MMC). MMC is one most polluted megacities world, with population 22 million residents, many whom unaware brain caused by their atmosphere. Fatal diseases (such Alzheimer’s Parkinson’s) that begin childhood populations living air environments preventable. We conclude UFPM/NPs capable disrupting neural homeostasis give rise relentless processes throughout entire life highly MMC. The paradigm reaching old age neurodegeneration no longer supported. Neurodegenerative changes start early pediatric ages irreversible. It time invest preventive medicine.

Language: Английский

Citations

0
Transcriptome analysis reveals that the injection of mesenchymal stem cells remodels extracellular matrix and complement components of the brain through PI3K/AKT/FOXO1 signaling pathway in a neuroinflammation mouse model DOI Creative Commons

Zhihao Xu,

Keqin Liu,

Guoqing Zhang

et al.

Genomics, Journal Year: 2025, Volume and Issue: 117(3), P. 111033 - 111033

Published: March 22, 2025

Language: Английский

Citations

0
Nitric oxide and experimental autoimmune encephalomyelitis review DOI Creative Commons

Maria Staykova,

Anne Bruestle

Journal of Neuroimmunology, Journal Year: 2025, Volume and Issue: unknown, P. 578586 - 578586

Published: April 1, 2025

Language: Английский

Citations

0
Melatonin Promotes Cerebral Angiogenesis in Ischemic Mice via BMP6/Smad1/5/9 Pathway DOI Creative Commons
Linlin Li,

Yujia Yuan,

Cong Zhang

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 25, 2025

Angiogenesis facilitates the reinstatement of blood supply to cerebral tissues after stroke by reconstructing vascular network, thereby rescuing penumbra region and restoring neural functions. Melatonin can modulate angiogenesis under a variety biological disease-related states, bone morphogenetic protein 6 (BMP6) targets regulators associated with angiogenesis. The specific functions melatonin BMP6 in following infarction, along potential intrinsic regulatory interactions between them, are currently unclear need further investigation. was given mice from 1st day through 28th post permanent distal middle artery occlusion (dMCAO). Our research revealed that enhanced neurological performance decreased size brain infarction. Additionally, it boosted circulation fostered area. Meanwhile, facilitated endothelial cells migration tube formation oxygen-glucose deprivation (OGD). promoted expression its downstream targets, Smad1/5/9, as well factors Vascular Endothelial Growth Factor (VEGF) Angiopoietin-1 (Ang1) vivo vitro, which counteracted or partially inhibited suppression expression. provides strong evidence promotes infarction BMP6/Smad1/5/9 signaling pathway, supporting restoration function.

Language: Английский

Citations

0