Mito-TEMPO

MitoTEMPO is a mitochondria-targeted antioxidant. MitoTEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. MitoTEMPO regulates Ca²⁺ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. MitoTEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. MitoTEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke^[1][2][3][4]. In Vitro:MitoTEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome and protects human podocytes (HPC) from TNF-α-induced injury^[1].
MitoTEMPO (200 μM; 24 h) improves mitochondrial function and induces PINK1/Parkin pathway-mediated mitophagy in TNF-α-injured human podocytes (HPC)^[1].
MitoTEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome in TNF-α-injured human podocytes (HPC) in a Parkin-dependent manner^[1].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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:MitoTEMPO (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].
MitoTEMPO (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].
MitoTEMPO (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].