时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Symbols (*, †, ‡, §) indicate significance (at 0.05 level) To verify whether the OVe−Mfn2 gene could protect mitochondria against IR-induced damage, the ADMS/GC-1 cells were categorized as B1 (ADMSC)/C1 (GC-1), B2 (ADMSC + IR)/C2 (GC-1 spg + IR), B3 [Mfn2 gene over expression in ADMSCs (ADMSCOVe−Mfn2 + IR)]/C3 (GC-1 spgOVe−Mfn2 + IR) and B4 (siRNA-Mfn2 in ADMSCs + IR)/C4 (siRNA-Mfn2 in GC-1 spg + IR).IF microscopy revealed that the number of mitochondrial cytochrome C-positive cells was greater in B1/C1, lowest on B4/C4 and significantly greater on B3/C3 than in B2/C2.；To determine whether ADMSCOVe−Mfn2 treatment would still maintain reproductive capacity in the context of TTIR, the molecular-cellular levels of RA were evaluated in testicular tissue.IHC staining and Western blot analyses revealed that the cellular and protein levels of RA were the highest in group 1, lowest in group 2, significantly higher in group 4 than in groups 3 and 5, and significantly higher in group 3 than in group 5.The presence of vimentin filaments and Sertoli cells is also a powerful tool for the prediction of spermatogenic function.；Fourth, reproductive functional outcomes, such as sperm quality and fertility, were not evaluated; therefore, whether the observed structural and molecular protection translates into functional recovery of reproductive capacity remains to be determined.In conclusion, the results of this study demonstrated that ADMSCOVe−Mfn2 was superior to ADMSC in terms of salvaging the testicular anatomical structure and reproductive system through MAPK-Mfn2 axial signaling-mediated restoration of mitochondrial biogenesis.Supplementary Information Supplementary Material 1: Supplementary Fig. 1.
方法
Previous epidemiological studies have reported that TT occurs in approximately one in 4000 males per year until the age of 25 years [1, 5] Pathologically, TT, called a twisted spermatic cord, results in reduced blood flow to the testis as a consequence of tissue ischemia [1–6] and potentially serious sequelae of infertility and subfertility; thus, rapid diagnosis and prompt treatment are critical for salvaging the testis [7–9].；Accordingly, prior to developing a safe and promising treatment for reperfusion-induced testicular injury for TT patients, fully delineating the underlying molecular–cellular mechanism of TT-induced reperfusion injury is important.Physiologically, adenosine triphosphate (ATP) is the main source of energy for cellular metabolic requirements; ATP is stored in mitochondria (i.e., energy-generating organelles called energy power generators) and is always produced through oxidative phosphorylation and substrate-level phosphorylation [17–19].；The cells were maintained in a proliferative, undifferentiated state by culture in high-glucose DMEM (11965-084; Gibco) at 37 °C in a humidified atmosphere containing 5% CO2.
核心结论
On the other hand, studies have demonstrated that silencing Mfn2 markedly impaired mitophagy and caused the accumulation of damaged mitochondria, resulting in increased ROS levels and ROS-induced apoptosis and death [26–29].；Studies have further shown that Mfn2 overexpression is associated with the activation of AMPK/Sirt3 signaling [32], resulting in the alleviation of cell injury caused by mitochondrial damage and the upregulation of mitochondrial fusion [32].Several studies have demonstrated that mesenchymal stem cells (MSCs) possess potent anti-inflammatory, immunomodulatory, antioxidative, and tissue-regenerative properties, making them attractive candidates for regenerative therapy [34, 35].；Importantly, our previous study [6] demonstrated that ADMSC therapy effectively protected the testis against testicular torsion-induced ischemia–reperfusion injury, supporting the rationale for utilizing ADMSCs as a therapeutic platform in the present investigation.
局限
However, effective pharmaceutics for avoiding gonad damage from IR are lacking because the central pathological mechanisms of testicular injury following TT have not been fully investigated [6, 15, 16].；However, these parameters were significantly reversed in EF4/F4.；However, these molecular–cellular perturbations were substantially attenuated in TTIR animals that received ADMSC treatment and were further substantially attenuated in TTIR animals that received ADMSCOVe−Mfn2 treatment.In the present in vivo study, compared with those in the SC group, the expression levels of fusion proteins (i.e., Mnf2 and OPA1) in the TTIR group were notably reduced, whereas the expression levels of fission proteins (i.e., PINK1 and PARKIN) and autophagic biomarkers (i.e., the ratio of LC3B-II to LC3B-I) were notably increased.
对本项目的价值
中高价值：属「干细胞 / 部分重编程与再生」方向；干细胞 / 再生 / 重编程栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.3/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 67,967 字符，题名指纹 0.96，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：脂肪组织间充质干细胞过表达 Mitofusin-2 经 AMPK 激活保全线粒体稳态，抵御睾丸扭转缺血再灌注损伤
- 英文标题：Mitofusin-2 overexpression in adipose tissue-derived mesenchymal stem cells protects the testis against testicular torsion-induced ischemia-reperfusion injury through preservation of mitochondrial homeostasis associated with AMPK activation.
- 期刊与标识：Stem cell research & therapy · PMID 42972475 · DOI 10.1186/s13287-026-05196-x · PMC PMC13725951