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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2020 Nov 24;41(1):446–457. doi: 10.1161/ATVBAHA.120.314944

Figure 6: Modulation of autophagy independent of changes in TERT activity determines the mechanism of FMD in non-CAD and CAD arterioles.

Figure 6:

(A, B) Activation of autophagy with TSA (A) or trehalose (B), despite inhibition of TERT activity with BIBR 1532, maintains NO as the primary mechanism of dilation in non-CAD adipose arterioles; (C) Inhibition of autophagy with BAFA1 despite activation of TERT activity with AGS 499 maintains H2O2 as the primary mechanism of dilation in CAD arterioles. (D) Smooth muscle responses to papaverine are not different with incubation with modulators of autophagy and telomerase. * P < 0.05 vs. control; TSA, trichostatin A; BAFA1, bafilomycin A1; L-NAME, NG-Nitro-l-arginine methyl ester; Peg-Cat; polyethylene glycol-catalase.