Ask about this productRelated genes to: TFAM antibody
- Gene:
- TFAM NIH gene
- Name:
- transcription factor A, mitochondrial
- Previous symbol:
- TCF6, TCF6L2
- Synonyms:
- -
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: TFAM antibody
Related articles to: TFAM antibody
- Traumatic brain injury (TBI) triggers complex and evolving secondary cascades that disrupt mitochondrial homeostasis and contribute to progressive neurodegeneration. Although mitochondrial impairment is a well-recognized driver of post-traumatic pathology, the spatial and temporal progression of mitochondrial dysfunction, particularly in regions distal to the injury site, remains poorly defined, and potential sex-specific responses remain understudied. Here, we performed a comprehensive mitochondrial-focused analysis in a mouse model of controlled cortical impact (CCI), quantifying mtDNA copy number (mtDNA-CN), mitochondrial gene expression, and protein markers regulating biogenesis, transcription, electron transport chain integrity, and mitophagy. Mitochondrial profiles were assessed across four brain regions (cortex at 2, 4, and 6 mm from the injury epicenter, and hippocampus) at four time points (6h, 12h, 24h, and 48h) in both female and male C57BL/6J mice. While mtDNA content exhibited only modest and region-restricted reduction, particularly near the injury core, transcriptional and protein-level changes were far more pronounced and sex-divergent. Females displayed extensive early cortical gene activation followed by widespread hippocampal suppression at 48 h across mitochondrial dynamics, OXPHOS, transcriptional regulation, and biogenesis pathways, accompanied by 48h in PGC-1α, TFAM, and NDUFS1. In contrast, males showed minimal transcriptional disruption but demonstrated delayed compensatory increases in TFAM, NDUFS1, and p62 protein levels, suggesting activation of mitochondrial maintenance and recovery programs. These spatially and temporally distinct responses reveal fundamental sex-specific vulnerabilities in mitochondrial regulation after TBI. Together, our findings provide a direction to an integrated mitochondrial landscape of early post-injury events and identifies critical windows and pathways that may support sex-specific therapeutic targeting to restore mitochondrial function after TBI. - Source: PubMed
Publication date: 2026/04/23
Vekaria Hemendra JPandya Chirayu DPrajapati PareshMoallem Elika ZVelmurugan Gopal VHubbard W BradBachstetter Adam DSullivan Patrick G - Silicosis is an irreversible, progressive occupational lung disease caused by chronic inhalation of crystalline silica (SiO₂), with no approved disease-modifying therapies currently available. Its pathological hallmark is a hostile fibrotic microenvironment driven by excessive reactive oxygen species (ROS), chronic inflammation, and mitochondrial dysfunction in alveolar epithelial type 2 (AEC2) cells; this microenvironment is the primary bottleneck for stem cell-based silicosis therapy, as it severely impairs the engraftment of exogenous AEC2 cells. Metformin (Met) exerts mitochondria-protective effects to preserve AEC2 function, but its clinical translation for silicosis is limited by low oral bioavailability and non-specific systemic distribution. Here, we developed a ROS-responsive biomimetic liposome (TK-PSBs@Met, also termed TPM NPs) for targeted Met delivery to AEC2s in fibrotic lungs, via a design combining pulmonary surfactant (PS)-mediated AEC2 targeting and thioketal (TK)-based ROS-triggered on-demand drug release. In vitro, TPM NPs reversed SiO₂-induced epithelial-mesenchymal transition (EMT), suppressed fibrotic and inflammatory responses, and restored mitochondrial function in A549 cells, a well-established AEC2 cell model. In vivo, TPM NPs significantly boosted the functional engraftment of TdTomato⁺ AEC2 stem cells, promoted alveolar regeneration, and attenuated collagen deposition and inflammation in SiO₂-induced silicosis mice. Mechanistically, TPM NPs mitigated silicotic fibrosis via a dual synergistic mechanism: remodeling the hostile fibrotic microenvironment and activating the AMPK/PGC-1α/NRF1/TFAM signaling axis to restore AEC2 mitochondrial biogenesis. Collectively, this TPM NP-AEC2 combinatorial therapy offers a translatable precision strategy for silicosis treatment and establishes a new paradigm for nanomedicine-augmented stem cell therapy in refractory fibrotic lung diseases. - Source: PubMed
Publication date: 2026/04/30
Zhang WenyueYang AnningGuo YiBao RuiZou SiweiAn RanPang YuanyuanXiao MengsiZhang HuningChang SirongJiang YidengLiu ZhihongSun Yue - This systematic review and meta-analysis explored the efficacy of Hyperbaric oxygen therapy (HBOT) in preclinical models of Alzheimer's disease (AD) and Parkinson's disease (PD). - Source: PubMed
Publication date: 2026/04/30
Radhakrishnan AiswaryaDutta DebprasadSaha MoupaliVenkatakrishnan SrikantKulkarni AkshayChandrachari Komal PrasadSalins Paul CSuresh Amritha - Studies have demonstrated that insults during development increase the risk for developing diseases later in life, including hypertension, ischemic heart disease, stroke, respiratory disease, diabetes, cancer, as well as psychiatric disorders. Hence, as mitochondrial dysfunction-induced oxidative stress has been proposed to be a central molecular hub linking metabolic and oxidative stress pathways, the serotonin modulation-related mitochondrial boost might mitigate such impairments. Thus, the present study investigates the effects of serotonina modulation by uoxetine on oxidative stress and mitochondrial biogenesis biomarkers in the brainstem and heart of male rats that were overfed during lactation period. - Source: PubMed
Publication date: 2026/04/13
de Lemos Maria Daniele Teixeira Beltrãode Sousa Fernandes Matheus SantosRodrigues Thyago de OliveiraLima de Souza VanessaYagin Fatma HilalCássia de Andrade Silva SeverinaHenrique Dos Santos Junior OsmarJosé Soares Ferreira DiorginisAldhahi Monira ILagranha Claudia J - Early brain injury (EBI) occurring within the first 72 h is a critical determinant of outcome after subarachnoid hemorrhage (SAH), yet effective treatments remain limited. Ferroptosis and mitochondrial dysfunction are central mechanisms in EBI. This study investigated whether deferoxamine (DFO), a clinically approved iron chelator, alleviates EBI after SAH via ferroptosis inhibition and mitochondrial restoration. - Source: PubMed
Publication date: 2026/04/26
Liu GuodongShan WenZhang ZhiyuanWei WutingWei YuBai WanshanDai JingLin Yixing