FoxG1 as a Potential Therapeutic Target for Alzheimer's Disease: Modulating NLRP3 Inflammasome via AMPK/mTOR Autophagy Pathway
Cell Mol Neurobiol. 2024 Apr 17;44(1):35. doi: 10.1007/s10571-024-01467-4.ABSTRACTAn increasing body of research suggests that promoting microglial autophagy hinders the neuroinflammation initiated though the NLRP3 inflammasome activation in Alzheimer's disease (AD). The function of FoxG1, a crucial transcription factor involved in cell survival by regulating mitochondrial function, remains unknown during the AD process and neuroinflammation occurs. In the present study, we firstly found that Aβ peptides induced AD-like neuroinflammation upregulation and downregulated the level of autophagy. Following low-dose Aβ25-35 st...
Source: Cellular and Molecular Neurobiology - April 17, 2024 Category: Cytology Authors: Qi Yun Si-Fei Ma Wei-Ning Zhang Meng Gu Jia Wang Source Type: research
Calorie restriction anti-hypertrophic effects are associated with improved mitochondrial content, blockage of Ca < sup > 2+ < /sup > -induced mitochondrial damage, and lower reverse electron transport-mediated oxidative stress
In this study, we show that this dietetic intervention prevents cardiac protein elevation, avoids fetal gene reprogramming (atrial natriuretic peptide), and blocks the increase in heart weight per tibia length index (HW/TL) seen in isoproterenol-induced cardiac hypertrophy. Our findings suggest that calorie restriction inhibits cardiac pathological growth while also lowering mitochondrial reverse electron transport-induced hydrogen peroxide formation and improving mitochondrial content. Calorie restriction also attenuated the opening of the Ca2+-induced mitochondrial permeability transition pore. We also found that calorie...
Source: Free Radical Research - April 17, 2024 Category: Research Authors: Aline Maria Brito Lucas Plinio Bezerra Palacio Pedro Lourenzo Oliveira Cunha Heberty Tarso Facundo Source Type: research
Nerolidol rescues hippocampal injury of diabetic rats through inhibiting NLRP3 inflammasome and regulation of MAPK/AKT pathway
In conclusion, our study reveals for the first time that nerolidol can ameliorate hippocampal damage, neuroinflammation, synaptic, ER, and mitochondrial damage in diabetic rats. Furthermore, we suggest that nerolidol may inhibit NLRP3 inflammasome activation via MAPK and AKT signaling pathways. These findings provide a new experimental basis for the use of nerolidol to ameliorate diabetes-induced brain tissue damage and the associated disease. AbstractDespite the observation of diabetes-induced brain tissue damage and impaired learning and memory, the underlying mechanism of damage remains elusive, and effective, targeted ...
Source: BioFactors - April 17, 2024 Category: Biochemistry Authors: Yining Lei,
Manqin Li,
Xinran Liu,
Lu Zhang,
Ruyi Zhang,
Fei Cai Tags: RESEARCH ARTICLE Source Type: research
GSE250044 Identification of a chromatin-bound ERR α interactome network in mouse liver [RNA-Seq]
ConclusionsOur work unveils a repertoire of previously unknown transcriptional partners of ERR α comprised of chromatin modifiers and transcription factors thus advancing our knowledge of how ERRα regulates metabolic transcriptional programs. (Source: GEO: Gene Expression Omnibus)
Source: GEO: Gene Expression Omnibus - April 17, 2024 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research
GSE250043 Identification of a chromatin-bound ERR α interactome network in mouse liver [ChIP-Seq]
ConclusionsOur work unveils a repertoire of previously unknown transcriptional partners of ERR α comprised of chromatin modifiers and transcription factors thus advancing our knowledge of how ERRα regulates metabolic transcriptional programs. (Source: GEO: Gene Expression Omnibus)
Source: GEO: Gene Expression Omnibus - April 17, 2024 Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Mus musculus Source Type: research
Genes, Vol. 15, Pages 500: Biallelic NDUFA4 Deletion Causes Mitochondrial Complex IV Deficiency in a Patient with Leigh Syndrome
Eirik Frengen
Oxidative phosphorylation involves a complex multi-enzymatic mitochondrial machinery critical for proper functioning of the cell, and defects herein cause a wide range of diseases called &ldquo;primary mitochondrial disorders&rdquo; (PMDs). Mutations in about 400 nuclear and 37 mitochondrial genes have been documented to cause PMDs, which have an estimated birth prevalence of 1:5000. Here, we describe a 4-year-old female presenting from early childhood with psychomotor delay and white matter signal changes affecting several brain regions, including the brainstem, in addition to lactic and...
Source: Genes - April 17, 2024 Category: Genetics & Stem Cells Authors: Doriana Misceo Petter Str ømme Fatemeh Bitarafan Maninder Singh Chawla Ying Sheng Sandra Monica Bach de Courtade Lars Eide Eirik Frengen Tags: Article Source Type: research
V-set and immunoglobulin domain containing 4 inhibits oxidative stress, mitochondrial dysfunction, and inflammation to attenuate Parkinson's disease progression by activating the JAK2/STAT3 pathway
V-set and immunoglobulin domain containing 4 (VSIG4) inhibits neurological dysfunction, microglial M1 polarization, and inflammation to participate in the progression of neurological disorders, but evidence regarding Parkinson's disease (PD) is scarce. The present study intended to investigate the engagement of VSIG4 in PD progression, and the potential mechanism. (Source: Journal of Neuroimmunology)
Source: Journal of Neuroimmunology - April 17, 2024 Category: Allergy & Immunology Authors: Pingping Cai, Junmei Wang, Jiangtao Xu, Min Zhang, Xinxin Yin, Shengquan He, Jingcong Zhuang Source Type: research
CoVar: A generalizable machine learning approach to identify the coordinated regulators driving variational gene expression
We present CoVar, an ML-based framework that builds upon the properties of existing inference models, to find the central genes driving perturbed gene expression across biological states. Unlike differentially expressed genes (DEGs) that capture changes in individual gene expression across conditions, CoVar focuses on identifyingvariational genes that undergo changes in their expression network interaction profiles, providing insights into changes in the regulatory dynamics, such as in disease pathogenesis. Subsequently, it findscore genes from among the nearest neighbors of these variational genes, which are central to th...
Source: PLoS Computational Biology - April 17, 2024 Category: Biology Authors: Satyaki Roy Source Type: research
Focusing on mitochondria in the brain: from biology to therapeutics
AbstractMitochondria have multiple functions such as supplying energy, regulating the redox status, and producing proteins encoded by an independent genome. They are closely related to the physiology and pathology of many organs and tissues, among which the brain is particularly prominent. The brain demands 20% of the resting metabolic rate and holds highly active mitochondrial activities. Considerable research shows that mitochondria are closely related to brain function, while mitochondrial defects induce or exacerbate pathology in the brain. In this review, we provide comprehensive research advances of mitochondrial bio...
Source: Translational Neurodegeneration - April 17, 2024 Category: Neurology Source Type: research
Molecular targets of histone deacetylase inhibitors in neurodegeneration and neuroprotection
ConclusionsMitochondrial bioenergetics- and neuroinflammation-related molecular targets of HDACi may be the key to the use of HDACi therapy for neurodegenerative diseases.Purpose of reviewWe aimed to discover molecular targets of HDACi in progressive neurodegeneration and to use these targets in potential therapeutics to induce neuroprotection.Recent findingsHDACi reverse cellular pathology in a mechanism involving mitochondrial bioenergetics and neuroinflammation, and the result is alleviation of pathologic phenotypes of neurodegenerative diseases. (Source: Molecular and Cellular Toxicology)
Source: Molecular and Cellular Toxicology - April 17, 2024 Category: Cytology Source Type: research
ROS-Induced Gingival Fibroblast Senescence: Implications in Exacerbating Inflammatory Responses in Periodontal Disease
This study aimed to investigate the role and the mechanism of cellular senescence in periodontal disease. Using single-cell RNA sequencing, we first found the upregulated level of cellular senescence in fibroblasts and endothelial cells from inflamed gingival tissue. Subsequently, human gingival fibroblasts isolated from healthy and inflamed gingival tissues were labeled as H-GFs and I-GFs, respectively. Compared to H-GFs, I-GFs exhibited a distinct cellular senescence phenotype, including an increased proportion of senescence-associated β-galactosidase (SA-β-gal) positive cells, enlarged cell morphology, and significant...
Source: Inflammation - April 17, 2024 Category: Allergy & Immunology Source Type: research
Revisiting airway epithelial dysfunction and mechanisms in chronic obstructive pulmonary disease: Role of mitochondrial damage
Am J Physiol Lung Cell Mol Physiol. 2024 Apr 16. doi: 10.1152/ajplung.00362.2023. Online ahead of print.ABSTRACTChronic exposure to environmental hazards causes airway epithelial dysfunction, primarily impaired physical barriers, immune dysfunction, and repair or regeneration. Impairment of airway epithelial function subsequently leads to exaggerated airway inflammation and remodeling, the main features of chronic obstructive pulmonary disease (COPD). Mitochondrial damage has been identified as one of the mechanisms of airway abnormalities in COPD, which is closely related to airway inflammation and airflow limitation. In ...
Source: Am J Physiol Lung Ce... - April 16, 2024 Category: Respiratory Medicine Authors: Qinglan He Peijun Li Lihua Han Chen Yang Meiling Jiang Yingqi Wang Xiaoyu Han Yuanyuan Cao Xiaodan Liu Weibing Wu Source Type: research
A systematic review on the biochemical threshold of mitochondrial genetic variants
Genome Res. 2024 Apr 16. doi: 10.1101/gr.278200.123. Online ahead of print.ABSTRACTMitochondrial DNA (mtDNA) variants cause a range of diseases from severe pediatric syndromes to aging-related conditions. The percentage of mtDNA copies carrying a pathogenic variant, variant allele frequency (VAF), must reach a threshold before a biochemical defect occurs, termed the biochemical threshold. Whether the often-cited biochemical threshold of >60% VAF is similar across mtDNA variants and cell types is unclear. In our systematic review, we sought to identify the biochemical threshold of mtDNA variants in relation to VAF by hum...
Source: Cell Research - April 16, 2024 Category: Cytology Authors: Karan K Smith Jesse D Moreira Callum R Wilson June O Padera Ashlee N Lamason Liying Xue Deepa M Gopal David B Flynn Jessica L Fetterman Source Type: research
Revisiting airway epithelial dysfunction and mechanisms in chronic obstructive pulmonary disease: Role of mitochondrial damage
Am J Physiol Lung Cell Mol Physiol. 2024 Apr 16. doi: 10.1152/ajplung.00362.2023. Online ahead of print.ABSTRACTChronic exposure to environmental hazards causes airway epithelial dysfunction, primarily impaired physical barriers, immune dysfunction, and repair or regeneration. Impairment of airway epithelial function subsequently leads to exaggerated airway inflammation and remodeling, the main features of chronic obstructive pulmonary disease (COPD). Mitochondrial damage has been identified as one of the mechanisms of airway abnormalities in COPD, which is closely related to airway inflammation and airflow limitation. In ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - April 16, 2024 Category: Cytology Authors: Qinglan He Peijun Li Lihua Han Chen Yang Meiling Jiang Yingqi Wang Xiaoyu Han Yuanyuan Cao Xiaodan Liu Weibing Wu Source Type: research
A crazy trio in Parkinson's disease: metabolism alteration, α-synuclein aggregation, and oxidative stress
Mol Cell Biochem. 2024 Apr 16. doi: 10.1007/s11010-024-04985-3. Online ahead of print.ABSTRACTParkinson's disease (PD) is an aging-associated neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the pars compacta of the substantia nigra and the presence of Lewy bodies containing α-synuclein within these neurons. Oligomeric α-synuclein exerts neurotoxic effects through mitochondrial dysfunction, glial cell inflammatory response, lysosomal dysfunction and so on. α-synuclein aggregation, often accompanied by oxidative stress, is generally considered to be a key factor in PD pathology...
Source: Molecular and Cellular Biochemistry - April 16, 2024 Category: Biochemistry Authors: Sheng Li Yanbing Liu Sen Lu Jiayi Xu Xiaokun Liu Di Yang Yuxuan Yang Lin Hou Ning Li Source Type: research
