Neuroimmune interactions in cardiovascular diseases
AbstractOur body is continuously in contact with external stimuli that need a fine integration with the internal milieu in order to maintain the homoeostasis. Similarly, perturbations of the internal environment are responsible for the alterations of the physiological mechanisms regulating our main functions. The nervous system and the immune system represent the main interfaces between the internal and the external environment. In carrying out these functions, they share many similarities, being able to recognize, integrate, and organize responses to a wide variety of stimuli, with the final aim to re-establish the homoeo...
Source: Cardiovascular Research - May 27, 2020 Category: Cardiology Source Type: research
Neuroimmune interactions in cardiovascular diseases
(Source: Cardiovascular Research)
Source: Cardiovascular Research - May 27, 2020 Category: Cardiology Source Type: research
Cyclophilin D palmitoylation and permeability transition: a new twist in the tale of myocardial ischaemia –reperfusion injury
This editorial refers to ‘Cysteine 202 of cyclophilin D is a site of multiple post-translational modifications and plays a role in cardioprotection’ by G. Amanakiset al., pp. 212 –223. (Source: Cardiovascular Research)
Source: Cardiovascular Research - May 25, 2020 Category: Cardiology Source Type: research
Human influenza A virus causes myocardial and cardiac-specific conduction system infections associated with early inflammation and premature death
ConclusionHuman IAV can infect the heart and cardiac-specific conduction system, which may contribute to cardiac complications and premature death. (Source: Cardiovascular Research)
Source: Cardiovascular Research - May 20, 2020 Category: Cardiology Source Type: research
Failure to vasodilate in response to salt loading blunts renal blood flow and causes salt-sensitive hypertension
ConclusionWe conclude that failure to vasodilate in response to salt loading causes SS hypertension by restricting renal perfusion and reducing renal NO through a mechanism involving NKCC2 in a mouse model of vascular peroxisome proliferator-activated receptor γ impairment. (Source: Cardiovascular Research)
Source: Cardiovascular Research - May 19, 2020 Category: Cardiology Source Type: research
