Research progress of PPARγ regulation of cholesterol and inflammation in Alzheimer's disease

Gu, Lili; Ju, Yue; Hu, Min; Zheng, Mianping; Li, Qin; Zhang, Xinyue

doi:10.1007/s11011-022-01139-6

Cited by 4 publications

(1 citation statement)

References 145 publications

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“…Notably, both APOE and PPARG were found to be differentially expressed in astrocytes between LOAD cases and controls. Numerous studies have considered the role of PPARG in the development of AD, 53–55 and indeed PPARG agonists have been evaluated as potential repurposed drugs to delay the onset of LOAD 56,57 . IRF7 is a TF that is a master regulator of type I interferons (IFNs) after activation by pathogen recognition receptors and was reported to be associated with decreased levels in LOAD brains relative to controls, supporting a hypothesis that the innate immune system is impaired in LOAD.…”

Section: Narrativementioning

confidence: 99%

Bioinformatics pipeline to guide post‐GWAS studies in Alzheimer's: A new catalogue of disease candidate short structural variants

Lutz

Chiba‐Falek

2023

Alzheimer's & Dementia

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BackgroundShort structural variants (SSVs), including insertions/deletions (indels), are common in the human genome and impact disease risk. The role of SSVs in late‐onset Alzheimer's disease (LOAD) has been understudied. In this study, we developed a bioinformatics pipeline of SSVs within LOAD–genome‐wide association study (GWAS) regions to prioritize regulatory SSVs based on the strength of their predicted effect on transcription factor (TF) binding sites.MethodsThe pipeline utilized publicly available functional genomics data sources including candidate cis‐regulatory elements (cCREs) from ENCODE and single‐nucleus (sn)RNA‐seq data from LOAD patient samples.ResultsWe catalogued 1581 SSVs in candidate cCREs in LOAD GWAS regions that disrupted 737 TF sites. That included SSVs that disrupted the binding of RUNX3, SPI1, and SMAD3, within the APOE‐TOMM40, SPI1, and MS4A6A LOAD regions.ConclusionsThe pipeline developed here prioritized non‐coding SSVs in cCREs and characterized their putative effects on TF binding. The approach integrates multiomics datasets for validation experiments using disease models.

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Section: Narrativementioning

confidence: 99%

Bioinformatics pipeline to guide post‐GWAS studies in Alzheimer's: A new catalogue of disease candidate short structural variants

Lutz

Chiba‐Falek

2023

Alzheimer's & Dementia

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Advances in Alzheimer's disease: A multifaceted review of potential therapies and diagnostic techniques for early detection

Sharma,

Pal,

Gupta

2024

Neurochemistry International

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Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders

Lee,

Yang,

Yang

2024

Cell Commun Signal

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The activation of peroxisome proliferator-activated receptor (PPAR)-γ has been extensively shown to attenuate inflammatory responses in conditions such as asthma, acute lung injury, and acute respiratory distress syndrome, as demonstrated in animal studies. However, the precise molecular mechanisms underlying these inhibitory effects remain largely unknown. The upregulation of heme oxygenase-1 (HO-1) has been shown to confer protective effects, including antioxidant, antiapoptotic, and immunomodulatory effects in vitro and in vivo. PPARγ is highly expressed not only in adipose tissues but also in various other tissues, including the pulmonary system. Thiazolidinediones (TZDs) are highly selective agonists for PPARγ and are used as antihyperglycemic medications. These observations suggest that PPARγ agonists could modulate metabolism and inflammation. Several studies have indicated that PPARγ agonists may serve as potential therapeutic candidates in inflammation-related diseases by upregulating HO-1, which in turn modulates inflammatory responses. In the respiratory system, exposure to external insults triggers the expression of inflammatory molecules, such as cytokines, chemokines, adhesion molecules, matrix metalloproteinases, and reactive oxygen species, leading to the development of pulmonary inflammatory diseases. Previous studies have demonstrated that the upregulation of HO-1 protects tissues and cells from external insults, indicating that the induction of HO-1 by PPARγ agonists could exert protective effects by inhibiting inflammatory signaling pathways and attenuating the development of pulmonary inflammatory diseases. However, the mechanisms underlying TZD-induced HO-1 expression are not well understood. This review aimed to elucidate the molecular mechanisms through which PPARγ agonists induce the expression of HO-1 and explore how they protect against inflammatory and oxidative responses.

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Research progress of PPARγ regulation of cholesterol and inflammation in Alzheimer's disease

Cited by 4 publications

References 145 publications

Bioinformatics pipeline to guide post‐GWAS studies in Alzheimer's: A new catalogue of disease candidate short structural variants

Bioinformatics pipeline to guide post‐GWAS studies in Alzheimer's: A new catalogue of disease candidate short structural variants

Advances in Alzheimer's disease: A multifaceted review of potential therapies and diagnostic techniques for early detection

Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders

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