Airborne stressors such as ambient air pollution, including particulate matter and allergens not only directly compromise pulmonary health by promoting chronic airway inflammation, bronchial obstruction or airway hyperresponsiveness but also facilitate the development of chronic systemic inflammation that may compromise tissue integrity of other vital organs. While respiratory tract responses to airborne stressors may appear as recognizable consequences, such as sneezing, coughing or wheezing, effects on other tissues may go unnoticed. Particularly, compromised cerebro- and cardiovascular health in response to acute and chronic exposures to airborne stressors highlights the health risks of ambient air pollution also with respect to stroke. However, mechanistic insights into how exposures to airborne stressors contribute to increased occurrence of cerebrovascular events or worsen their outcome are not yet available. 

According to the World Health Organization, most people consume too much salt - on average 9–12 grams per day, which is around twice the recommended maximum level of intake. Excess dietary sodium has been linked to elevations in blood pressure, and recent pre-clinical and clinical data support that even in the absence of an increase in blood pressure, excess dietary salt can adversely affect target organs, including the blood vessels, heart, kidneys, and brain. 

Notably, epidemiological studies have suggested sex-specific differences, with a higher prevalence of salt sensitivity observed in women compared to men. However, knowledge of salt-sensitive mechanisms is largely restricted to males, while female-specific studies on the topic are scarce. 

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) regulate islet function, nutrient absorption, appetite, and energy homeostasis, making them potential diabetes treatments. G-protein coupled receptors for these peptides are also expressed in the cardiovascular system, sparking interest in their relevance to cardiovascular disease (CVD). Most research has focused on GLP-1, with clinical trials showing its benefits beyond blood glucose control. However, with increasing use of dipeptidyl peptidase-4 (DPP-4) inhibitors, which elevate both GLP-1 and GIP levels, understanding GIP's cardiovascular effects is crucial. DPP-4 inhibitors have been linked to increased heart failure risk in some patients. The newest dual GIP and GLP-1 receptor agonists heighten the need to understand GIP's potential adverse effects on CVD.