Ask about this productRelated genes to: TFAM Blocking Peptide
- 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 Blocking Peptide
Related articles to: TFAM Blocking Peptide
- Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide and the leading cause of dementia. Mitochondrial dysfunction is a key pathogenic event that drives neuronal damage and disease progression. Thus, protecting against mitochondrial damage in neuronal cells has become a critical therapeutic target for AD prevention and treatment. Our previous research has shown that artemether can protect PC12 cells from oxidative stress damage induced by Aβ and oxygen-glucose deprivation, but its underlying regulatory mechanisms remain elusive. Therefore, it is essential to elucidate the role and mechanism of artemether in Aβ-induced mitochondrial damage. - Source: PubMed
Publication date: 2026/09/04
Cai JunLuo JingyiCai YongguXu YueRan RensenXiao MeijunYe QiaoyuanZheng WenhuaLi Shuai - Mitochondrial targeting represents a promising antitumor strategy by modulating cell differentiation, metabolic reprogramming, and immune responses. While chlorogenic acid (CGA) has demonstrated the ability to induce tumor cell differentiation and enhance antitumor immunity, the involvement of mitochondrial regulation in these effects remains unclear. This study investigated whether CGA mediates antitumor immune effects through mitochondrial regulation, thereby providing a theoretical framework for natural product-based, mitochondria-targeted therapies. Our findings reveal that CGA inhibits the translocation of mitochondrial transcription factor A (TFAM) into the mitochondria and promotes mtDNA leakage by disrupting the ATF5-mtHSP70 signaling axis. The cytosolic leakage of mtDNA activates the cGAS/STING pathway, triggering the activation of natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), which ultimately facilitates antitumor immunity. In a mouse model, ATF5 knockout enhances cGAS/STING signaling and subsequent immune responses, leading to tumor growth inhibition. These results highlight a novel role of CGA in regulating mitochondrial-associated proteins, positioning it as a potential therapeutic strategy for cancer via the mtDNA-cGAS-STING pathway. - Source: PubMed
Publication date: 2026/08/12
Li RuiZhou PingHu Chu-JuanSi GeRen LingCui Jin-JinHe Ying-YingHan Yan-XingZhang JieLi Wen-BinWang Lu-LuJiang Jian-Dong - Mitochondrial dysfunction is one of the significant aspects of Parkinson's disease (PD) pathophysiology, marked by a gradual decline in oxidative phosphorylation, an abnormal increase in free radical species, dysfunctional mitochondrial quality control, and faulty mitochondrial biogenesis. Sirtuin 1 (SIRT1), a NAD-dependent class-III deacetylase, acts as a crucial metabolic sensor that orchestrates transcriptional programs related to mitochondrial biogenesis, respiratory chain assembly, and stress resilience, mainly by way of deacetylation and activation of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α). While screening for the small molecule activators, we have identified that 2,4-dihydroxy-Azaflavanone allosterically activates SIRT1. This chapter outlines a detailed, multi-layered methodological framework for assessing the allosteric activation of SIRT1 by 2,4-dihydroxy-azaflavanone and its downstream effects in a cellular models of PD. The validation process involves synthesis of small molecules, molecular docking studies utilizing crystallographic SIRT1 coordinates (PDB: 5BTR), in vitro fluorometric deacetylase assays with recombinant enzyme, and cellular thermal shift assays (CETSA) to confirm direct, isoform-selective target engagement. The activation of downstream pathways is evaluated by immunoblotting and quantitative PCR for PGC-1α, TFAM, and quantification of mitochondrial DNA (mtDNA) copy number. Functional restoration of mitochondria in cells is analyzed by assessing the overall mitochondrial bioenergetics parameters using Seahorse extracellular flux analyzer. Overall, this integrated approach offers robust, reproducible results for exploring SIRT1-activators in the mechanisms mediating neurodegenerative disease models. - Source: PubMed
Publication date: 2026/07/02
Pant ChitrakshiAlli Vidya JyothiSukumar GenjiMohapatra AbhijitJadav Surender SinghPabbaraja SrihariKalivendi Shasi V - Aging is characterized by progressive cognitive decline and metabolic dysregulation, contributing to increased vulnerability to age-related disorders. β-position palmitic acid -containing structured lipids (sn-2 palmitate), naturally enriched in human milk fat, have been reported to modulate inflammation and lipid metabolism. However, whether sn-2 palmitate-rich lipids exert beneficial effects beyond early development, particularly in the context of aging-related decline, remains unclear; further, its effects in aged populations or senescence models remain largely unknown. Therefore, we investigated the potential anti-aging effects of sn-2 palmitate-enriched lipid in senescence-accelerated mouse prone 8 (SAMP8)-a model of age-related functional decline. Eight-week-old SAMP8 mice were fed a sn-2 palmitate-enriched lipid supplemented diet for eight weeks. Behavioral tests, hippocampal biochemical analyses, and histological assessments were performed. sn-2 palmitate-enriched lipid supplementation significantly improved cognitive performance and reduced hippocampal expression of senescence markers (p16, p21) and pro-inflammatory cytokines (IL-6, TNF-α). Furthermore, sn-2 palmitate enhanced NAD⁺/NADH ratios and increased Sirt1/3 deacetylase activities, accompanied by upregulation of mitochondrial biogenesis-related factors (PGC-1α, NRF1, TFAM). These findings suggest that sn-2 palmitate-enriched lipid may attenuate aging-associated cognitive and physiological decline through modulation of NAD⁺ metabolism and mitochondrial function. - Source: PubMed
Publication date: 2026/09/03
Tsutsumi RieTanaka SaeFunatsu YuiMeta YoshihiroIzumi-Mishima YunaNomura KazuhiroSakaue Hiroshi - Septic cardiomyopathy (SCM) is a prevalent and serious cardiac complication arising from sepsis-induced multiple organ dysfunction syndrome (MODS). The pathogenesis of SCM is complex and primarily involves immune-inflammatory responses, oxidative stress, programmed cell death, and mitochondrial dysfunction. In recent years, mitochondrial quality control (MQC) has attracted growing interest as a central mechanism for maintaining cellular homeostasis and myocardial energy metabolism in SCM. This review systematically summarizes recent advances in four key MQC mechanisms involved in SCM: (1) phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy; (2) mitochondrial dynamics, including dynamin-related protein 1 (Drp1)/fission protein 1 (FIS1)-driven fission and optic atrophy protein 1 (OPA1)/mitofusin (MFN)-regulated fusion; (3) mitochondrial biogenesis under the regulatory control of the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α)/nuclear respiratory factor 1 (NRF1)/mitochondrial transcription factor A (TFAM) axis; and (4) the mitochondrial unfolded protein response (UPRmt), which maintains mitochondrial proteostasis through mediators such as C/EBP homologous protein (CHOP), YME1-like protease (YME1L), and Overlapping activity with m-AAA protease 1 (OMA1). These mechanisms have been shown to work synergistically to regulate mitochondrial clearance, renewal, and functional maintenance. Any imbalance among them can exacerbate myocardial injury. This review also emphasizes the redox crosstalk between oxidative stress and immune inflammation, with an emphasis on the pivotal contributions of NADPH oxidase 2 (NOX2), high mobility group box 1 (HMGB1), and the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in vascular endothelial dysfunction and cardiac depression. In conclusion, preserving the dynamic equilibrium of MQC is crucial for preventing or reversing SCM and may present novel molecular targets and therapeutic strategies. - Source: PubMed
Pu XiangyiYan ZhaoqiLiu ZhimingChang XingLiu Ruxiu