Definition, Classification, Diagnosis and Differential Diagnosis of
                    Diabetes Mellitus: Update 2023

Pleus, Stefan; Tytko, Andrea; Landgraf, Rüdiger; Heinemann, Lutz; Werner, Christoph; Müller-Wieland, Dirk; Ziegler, Anette-Gabriele; Müller, Ulrich A.; Freckmann, Guido; Kleinwechter, Helmut; Schleicher, Erwin; Nauck, Matthias; Petersmann, Astrid

doi:10.1055/a-2166-6643

Cited by 1 publication

(1 citation statement)

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“…Plaques that are prone to rupture are considered “vulnerable”, leading to the acute blockage of the artery and clinically to either acute ischemic heart attack or stroke [ 3 , 4 ]. The co-existence of diabetes mellitus (DM) multiplies the risk for acute plaque destabilization and consequent adverse cardiovascular events [ 5 , 6 ]. On the other hand, statins have been long proven to exert “pleiotropic” actions and remain an essential part of the secondary prevention of atherosclerotic cardiovascular diseases (ASCVDs).…”

Section: Introductionmentioning

confidence: 99%

The Anti-Atherosclerotic Effects of Endothelin Receptor Antagonist, Bosentan, in Combination with Atorvastatin—An Experimental Study

Stasinopoulou,

Kostomitsopoulos,

Kadoglou

2024

IJMS

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Bosentan, an endothelin receptor antagonist (ERA), has potential anti-atherosclerotic properties. We investigated the complementary effects of bosentan and atorvastatin on the progression and composition of the atherosclerotic lesions in diabetic mice. Forty-eight male ApoE−/− mice were fed high-fat diet (HFD) for 14 weeks. At week 8, diabetes was induced with streptozotocin, and mice were randomized into four groups: (1) control/COG: no intervention; (2) ΒOG: bosentan 100 mg/kg/day per os; (3) ATG: atorvastatin 20 mg/kg/day per os; and (4) BO + ATG: combined administration of bosentan and atorvastatin. The intra-plaque contents of collagen, elastin, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-a (TNF-a), matrix metalloproteinases (MMP-2, -3, -9), and TIMP-1 were determined. The percentage of lumen stenosis was significantly lower across all treated groups: BOG: 19.5 ± 2.2%, ATG: 12.8 ± 4.8%, and BO + ATG: 9.1 ± 2.7% compared to controls (24.6 ± 4.8%, p < 0.001). The administration of both atorvastatin and bosentan resulted in significantly higher collagen content and thicker fibrous cap versus COG (p < 0.01). All intervention groups showed lower relative intra-plaque concentrations of MCP-1, MMP-3, and MMP-9 and a higher TIMP-1concentration compared to COG (p < 0.001). Importantly, latter parameters presented lower levels when bosentan was combined with atorvastatin compared to COG (p < 0.05). Bosentan treatment in diabetic, atherosclerotic ApoE−/− mice delayed the atherosclerosis progression and enhanced plaques’ stability, showing modest but additive effects with atorvastatin, which are promising in atherosclerotic cardiovascular diseases.

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