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Additionally, the control plates showed that our chassis was able to uptake the DVK-AF plasmid (Figure 6.2) and was not naturally resistant (Figure 6.1)

Glossary AGEs Advanced Glycation End products AMPK AMP-activated protein kinase Arg1 Arginase 1 ASC Apoptosis-associated speck-like protein containing a CARD ATP Adenosine Triphosphate BA Baicalin BH4 Tetrahydrobiopterin CAT Catalase C-dots Carbon dots cGAS cyclic GMP-AMP Synthase Cyt c Cytochrome c DAMPs Damage-Associated Molecular Patterns DW Diabetic wounds DMM Dimethyl Malonate Drp1 Dynamin-related protein 1 ECM Extracellular Matrix EGF Epidermal Growth Factor EPCs Endothelial Progenitor Cells ETC Electron Transport Chain EVs Extracellular Vesicles Fenton reaction Fenton reaction GPx Glutathione Peroxidase GTP Guanosine Triphosphate HG HyperGlycemia HIF-1 Hypoxia-Inducible Factor 1-alpha IFN Interferon IB Inhibitor of Kappa B Alpha IL Interleukin iNOS inducible Nitric Oxide Synthase IRF3 Interferon Regulatory Factor 3 MAPK Mitogen-Activated Protein Kinase MDA Malondialdehyde Mfn1/2 Mitofusin 1/2 MMPs Matrix Metalloproteinases MOFs Metal-Organic Frameworks MPs Mitochondria-targeted Peptides mPTP mitochondrial Permeability Transition Pore MSCs Mesenchymal Stem Cells mtDNA mitochondrial DNA mtROS mitochondrial Reactive Oxygen Species NF-B Nuclear Factor Kappa B NLRP3 NLR Family Pyrin Domain Containing 3 NO Nitric Oxide Nrf2 Nuclear factor erythroid 2-related factor 2 OPA1 Optic Atrophy 1 OXPHOS OXidative PHOSphorylation PDGF Platelet-Derived Growth Factor PHD Prolyl Hydroxylase PINK1 PTEN-induced Kinase 1 RAGE Receptor for AGEs ROS Reactive Oxygen Species SDH Succinate Dehydrogenase SIRT1 Sirtuin 1 SOD Superoxide Dismutase STING Stimulator of Interferon Genes TCA Tricarboxylic Acid TGF- Transforming Growth Factor-Beta TIMPs Tissue Inhibitors of Metalloproteinases TNF- Tumor Necrosis Factor-Alpha TPP+ Triphenylphosphonium VEGF Vascular Endothelial Growth Factor m Mitochondrial Membrane Potential References 1 AkterS.AhmadS

When these mice where administered IGF-1 they showed lowered fasting glucose, and because no functional IGF-1R is present in muscle, such effect is believed to be due to renal gluconeogenesis suppression [129, 163]