Anna Gottschlich

Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes

Redox regulation of cardiovascular inflammation – Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species

Inflammaging: a new immune–metabolic viewpoint for age-related diseases

Reactive oxygen species (ROS) as pleiotropic physiological signalling agents

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

Artificial Intelligence in Cardiology

Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases

Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes

Reactive Oxygen Comes of Age: Mechanism-Based Therapy of Diabetic End-Organ Damage

Inflammageing and metaflammation: The yin and yang of type 2 diabetes

Gliptins Suppress Inflammatory Macrophage Activation to Mitigate Inflammation, Fibrosis, Oxidative Stress, and Vascular Dysfunction in Models of Nonalcoholic Steatohepatitis and Liver Fibrosis

Effects of empagliflozin on blood pressure and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes

Phenotype-Specific Treatment of Heart Failure With Preserved Ejection Fraction

The Sodium-Glucose Co-Transporter 2 Inhibitor Empagliflozin Improves Diabetes-Induced Vascular Dysfunction in the Streptozotocin Diabetes Rat Model by Interfering with Oxidative Stress and Glucotoxicity

Chronic therapy with isosorbide-5-mononitrate causes endothelial dysfunction, oxidative stress, and a marked increase in vascular endothelin-1 expression

Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Expression