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Fig. 3 | Cardiovascular Diabetology

Fig. 3

From: Dysregulated inflammation, oxidative stress, and protein quality control in diabetic HFpEF: unraveling mechanisms and therapeutic targets

Fig. 3

Protein kinase G Signaling Pathway in Inflammation in Left Ventricular Biopsies from Patients with HFpEF, with (+ DM) and without Concomitant Diabetes (-DM). A Schematic representation of the PKG signaling pathway. AKT: AKT serine/threonine kinase; cGMP: cyclic guanosine monophosphate; eNOS, endothelial nitric oxide synthase; GTP: guanosine triphosphate; NO: nitric oxide; PI3K: phosphatidylinositol-3-kinase; PIP2: phosphatidylinositol-4,5-bisphosphate; PIP3: phosphatidylinositol-3,4,5-trisphosphate; PKG: protein kinase G; sGC: soluble guanylyl cyclase. B Expression of eNOS over GAPDH. C NOS3 mRNA level. D NO level. E Activity of sGC. F Myocardial cGMP level. G PKG activity. H PRKG1 mRNA level. Data are represented as box and whisker plots (median, 25th to 75th percentiles, minimum, and maximum (n = 8–10 samples/group). P-values are derived from an unpaired t-test; * P < 0.05, ** P < 0.01

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Cardiovascular Diabetology

ISSN: 1475-2840