Ask about this productRelated genes to: SLC25A28 antibody
- Gene:
- SLC25A28 NIH gene
- Name:
- solute carrier family 25 member 28
- Previous symbol:
- -
- Synonyms:
- MRS3/4, MRS4L
- Chromosome:
- 10q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-19
- Date modifiied:
- 2016-02-18
Related products to: SLC25A28 antibody
Related articles to: SLC25A28 antibody
- Mitochondrial dysfunction plays a central role in the pathogenesis of bronchopulmonary dysplasia (BPD). Solute carrier family 25 member 28 (SLC25A28) is an iron transporter located in the inner mitochondrial membrane. In this study, we aimed to explore the role and underlying molecular mechanisms of SLC25A28 in BPD. Hyperoxia (85% O) was used to establish a neonatal murine model of BPD, and mouse lung epithelial cells (MLE-12 cells) were used in vitro. SLC25A28 expression and activity were downregulated under hyperoxic conditions, both in vivo and in vitro. SLC25A28 overexpression restored hyperoxia-induced mitochondrial oxidative phosphorylation (OXPHOS) dysfunction, and further enhanced the proportion of Ki67-positive cells by 37% ( < 0.05) and increased migration by 33% ( < 0.01) in MLE-12 cells. In contrast, SLC25A28 knockdown exacerbated these impairments in MLE-12 cells, with reduced the proportion of Ki67 positive cells by 71% ( < 0.01) and a 35% reduction in the migration rate. SLC25A28 was also knocked down in vivo, which further aggravated alveolar simplification in BPD mice. Furthermore, the mitochondrial-targeted peptide SS-31 could potentially interact with SLC25A28 and preserve its protein abundance. SS-31 administration mitigated hyperoxia-induced alveolar simplification, with the radical alveolar count (RAC) increasing by 28% ( < 0.05) and the mean linear intercept (MLI) decreasing by 20% ( < 0.001). In summary, this study revealed that SLC25A28 ameliorated hyperoxic lung injury by improving mitochondrial OXPHOS in alveolar epithelial cells, suggesting that it may serve as a potential therapeutic target for BPD. - Source: PubMed
Publication date: 2026/04/08
Lu TaoChen Shi-QiLi Shu-HongLi Sheng-PengWu Ya-XianPang Qing-FengChen Dan - Nitrite accumulation poses a significant threat to aquatic organisms in intensive aquaculture systems. Macrobrachium rosenbergii, a commercially vital freshwater prawn, exhibits adaptive responses to environmental stressors, yet the molecular mechanisms underlying nitrite tolerance remain poorly understood. This study employed integrated mRNA and miRNA transcriptomics to dissect the regulatory networks activated in M. rosenbergii hepatopancreas under acute nitrite stress (0, 40, and 87.25 mg/L nitrite-N over 48 h). High-throughput sequencing revealed 640 and 912 differentially expressed genes (DEGs) in low-concentration (LC) and high-concentration (HC) groups, respectively, compared to controls (CK). In the LC group, enrichment was predominantly observed in ribosome biogenesis (96 genes, p < 0.001). Conversely, the HC group was characterized by the significant modulation of the PPAR signaling (11 genes), glycerophospholipid metabolism, and the citrate cycle (p < 0.005). Calcium signaling and MAPK pathways may be central to stress adaptation across both groups. miRNA profiling revealed 17 downregulated and 2 upregulated miRNAs within the HC group relative to the CK group, with miR-193-y, miR-263-x, and miR-145-x implicated in metabolic regulation. Notably, novel miRNAs (e.g., novel-m0087-3p) showed concentration-dependent expression. qPCR validated the consistency of sequencing data, confirming stress-responsive genes (P53, HORMA, SLC25a28) and miRNAs. This study is the first to integrate the mRNA-miRNA regulatory network in Macrobrachium rosenbergii to elucidate the response mechanism to nitrite stress, emphasizing the role of metabolic reprogramming and signal pathway regulation as key survival strategies. It provides a foundation and novel perspectives for the molecular evolution of nitrite adaptability in aquatic animals and breeding programs. - Source: PubMed
Publication date: 2026/03/04
Li XilianCheng HaihuaFan YunpengXu BinpengXu YangGao Qiang - Postoperative cognitive dysfunction is a type of cognitive impairment that occurs after surgery. Here, this experiment investigated the role of PLCG1 in sevoflurane-induced model and the molecular mechanisms underlying its regulation of ferroptosis. Single-cell RNA sequencing data and bioinformatic analyses were performed using GEO datasets (GSE196239). Mice were exposed to 2.3% sevoflurane for 2 h daily for 3 consecutive days. PLCG1 expression was up-regulation in patients exposed to sevoflurane. Specifically, blood samples from these patients exhibited elevated levels of PLCG1 mRNA. Consistently, in a mouse model of sevoflurane exposure, both mRNA and protein levels of PLCG1 were significantlyincreased in brain tissue. Single-cell RNA sequencing analysis revealed that PLCG1 was predominantly expressed in astrocytes (marked by AQP4, GFAP, LUZP2, and SLC25A28) and neurons (marked by B3GAT2, ENO2, GNG2, and SLC1A1) in sevoflurane-exposed patients. In contrast, PLCG1 expression was undetectable in B cells (CD74, CD79B, CD80, CD86), T cells (CD4, CD8B, CD69, CD247), or macrophages (CD36, CD68, CD83, CD163). In conclusion, PLCG1 drives neuronal ferroptosis in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. In conclusion, PLCG1 drives neuronal in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A Ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. - Source: PubMed
Publication date: 2026/02/27
Chen JianCai YangWang JingruYue KunSun Yingying - Diabetes significantly increases the risk of Parkinson's disease (PD), and mitochondrial dysfunction is considered a shared pathological mechanism between diabetes and PD. Although our previous research indicated that shikonin ameliorates hyperglycemia-driven PD progression through dual regulation of glycolysis (via inhibition of pyruvate kinase muscle isozyme 2) and mitochondrial function, its mitochondrial repair mechanism remains unclear. Here, we demonstrate that shikonin repairs neuronal damage induced by high glucose and 6-hydroxydopamine via a PKM2-independent, p53/Solute Carrier Family 25 Member 28 (SLC25A28)-dependent mitochondrial iron shuttle. Proteomic analysis revealed that shikonin activates the SLC25A28-cytochrome c axis, maintaining mitochondrial Fe homeostasis. Molecular validation confirmed that shikonin directly binds to p53 (isothermal titration calorimetry K = 6.3 μM), promotes mitochondrial translocation of p53, and subsequently activates SLC25A28. This process facilitates Fe-dependent assembly of the cytochrome c/cytochrome c oxidase subunit 4 complex, restoring oxidative phosphorylation. Our work uncovers the p53/SLC25A28 axis as a target for shikonin-mediated mitochondrial iron homeostasis, providing a therapeutic strategy for diabetes-associated PD. - Source: PubMed
Publication date: 2026/01/20
Wang YanweiHan ZiweiPan ShanshanGuo MinsongWu MeihongLiu XuesongZhou YuanZhao JiahuiChen YongXu Tengfei - To investigate the causal relationship between mitochondrial genes and the pathogenesis of carotid plaque (CP), a multiomics-integrated Mendelian randomization (MR) analysis was performed in this study. - Source: PubMed
Publication date: 2025/11/01
Yu ZhuyuanMeng XiangyuanZong ZiyuSong QiHuo YingchaoChen Hao