Mito-TEMPO

Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca²⁺ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke^[1][2][3][4]. In Vitro:Mito-TEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome and protects human podocytes (HPC) from TNF-α-induced injury^[1].
Mito-TEMPO (200 μM; 24 h) improves mitochondrial function and induces PINK1/Parkin pathway-mediated mitophagy in TNF-α-injured human podocytes (HPC)^[1].
Mito-TEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome in TNF-α-injured human podocytes (HPC) in a Parkin-dependent manner^[1].
Mito-TEMPO (0.1-10 μM; 2 days) significantly reduces mitochondrial superoxide levels in bone marrow mesenchymal stem cells (BMSCs) of rats in the sham-operated group, short-term ovariectomized (ST-OVX) group, and long-term ovariectomized (LT-OVX) group, with the most prominent effect on BMSCs in the LT-OVX group at the concentration of 1 μM^[3].
Mito-TEMPO (1 μM; 7 days) upregulates the activity of alkaline phosphatase (ALP), an early osteogenic marker, in bone marrow mesenchymal stem cells (BMSCs) of rats with long-term ovariectomy (LT-OVX), and reverses the activity reduction caused by estrogen deficiency^[3].
Mito-TEMPO (1 μM; 2 days) alleviates premature senescence of bone marrow mesenchymal stem cells (BMSCs) in ovariectomized (LT-OVX) rats by reducing the expression of senescence markers, decreasing DNA damage, and ameliorating cell proliferation impairment^[3].
Mito-TEMPO (1 μM; 2 days) restores lysosomal acidity, reduces mature CTSB levels, and alleviates lysosomal dysfunction in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats induced by estrogen deficiency^[3].
Mito-TEMPO (1 μM; 2 days) enhances mitophagy in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats, which is evidenced by increased colocalization of mitochondrial markers and lysosomal markers^[3].
Mito-TEMPO (1 μM; 2 days) inhibits the activation of mitochondrial unfolded protein response (UPR_mt) in bone marrow mesenchymal stem cells (BMSCs) of ovariectomized (LT-OVX) rats induced by estrogen deficiency by reducing the expression of HSP60 and CLPP proteins^[3].
Mito-TEMPO (1 μM; 2 days) restores mitochondrial membrane potential in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats and alleviates estrogen deficiency-induced mitochondrial dysfunction^[3].
Mito-TEMPO (1 μM; 2 days) improves mitochondrial respiratory function, including basal respiration, ATP-coupled respiration, and maximal respiration, in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats^[3]. In Vivo:Mito-TEMPO (0.7 mg/kg; i.p.; once daily for 7 consecutive days) significantly improves renal function, alleviates podocyte injury, inhibits NLRP3 inflammasome activation, and induces PINK1/Parkin pathway-mediated mitophagy in rats with chronic kidney disease (CKD)^[1].
Mito-TEMPO (0.6 mg/kg; i.p.; once daily for 4 weeks) alleviates trabecular bone loss and reduces the expression of senescence and mitochondrial stress markers in ovariectomized rats with osteoporosis^[3].
Mito-TEMPO (0.7 mg/kg/day; i.p.; once daily for 14 consecutive days) exerts protective effects against ischemia-reperfusion-induced cardiac and neurological dysfunction in male Wistar albino rats, as evidenced by the normalization of hemodynamic, electrocardiographic, biochemical and histological parameters compared with the IR group^[4].