The precise mechanisms by which inhibition of SGLT2 reduces cardiovascular risk in humans are not entirely understood. The widely accepted hypothesis suggests that SGLT2i acts, mainly, by reducing the interstitial volume much greater than intravascular volume. Besides, EMPEROR-Reduced Trial does not support a dominant role of diuresis in mediating the physiological changes or clinical benefits of SGLT2 inhibitors during heart failure in patients with reduced ejection fraction. Short-term exposure to empagliflozin reduced patients' left ventricular mass index and myocardial fibrosis, rendering it difficult to assume that SGLT2 inhibition could not affect diabetic cardiomyocyte metabolism directly. However, human studies show that SGLT2s would not be expressed in the myocardium, but such results are limited and inconsistent. In addition, any role of SGLT2 inhibitors on development and worsening of atherosclerotic deserves further investigations.
Atherosclerotic plaques represent a nosographic entity, which, although much studied in terms of damage to the vessels, is still not a little so as regards their metabolism. Recent inhibitors of SGLT2 protein (SGLT2i) have been shown to play a significant role in heart failure therapy. Since heart failure is one of the most frequent complications of diabetes mellitus, and the link between diabetes mellitus and atherosclerosis is very well demonstrated, it cannot be excluded that the use of SGLT2i may have a double benefit both in terms of metabolic control and control of the atherosclerotic process at both a myocardial and vascular level. In fact, numerous studies have shown that atherosclerosis is a process that lowers a highly significant inflammatory burden and that SGLT2i may have some role in inflammation. It is not possible to exclude that, considering the absence of the SGLT2 protein at the level of cardiomyocytes, SGLT2i may have an anti-atherosclerotic role through an anti-inflammatory action on endothelial cells.
In this special issue, concerning the relationships between SGLT2i and atherosclerosis, topics that address the relationships between the use of SGLT2i and the genesis and progression of atherosclerosis both at the vascular and at the myocardial level would be very well considered. Also important, clinical data that are able to substantiate an anti-atherosclerotic role of SGLT2i. For this reason, studies "in vitro" (on cells or organoids) or "in vivo" (on animals and humans) seem to be of great use, being able to generate data that would be very useful to the entire scientific community. However, epidemiological studies or meta-analyses could also contribute to the advancement of knowledge in this field. Finally, review articles could make it possible to make a State of Art and to understand what is currently the degree of scientific knowledge of the problem that is the subject of the special issue.
The precise mechanisms by which inhibition of SGLT2 reduces cardiovascular risk in humans are not entirely understood. The widely accepted hypothesis suggests that SGLT2i acts, mainly, by reducing the interstitial volume much greater than intravascular volume. Besides, EMPEROR-Reduced Trial does not support a dominant role of diuresis in mediating the physiological changes or clinical benefits of SGLT2 inhibitors during heart failure in patients with reduced ejection fraction. Short-term exposure to empagliflozin reduced patients' left ventricular mass index and myocardial fibrosis, rendering it difficult to assume that SGLT2 inhibition could not affect diabetic cardiomyocyte metabolism directly. However, human studies show that SGLT2s would not be expressed in the myocardium, but such results are limited and inconsistent. In addition, any role of SGLT2 inhibitors on development and worsening of atherosclerotic deserves further investigations.
Atherosclerotic plaques represent a nosographic entity, which, although much studied in terms of damage to the vessels, is still not a little so as regards their metabolism. Recent inhibitors of SGLT2 protein (SGLT2i) have been shown to play a significant role in heart failure therapy. Since heart failure is one of the most frequent complications of diabetes mellitus, and the link between diabetes mellitus and atherosclerosis is very well demonstrated, it cannot be excluded that the use of SGLT2i may have a double benefit both in terms of metabolic control and control of the atherosclerotic process at both a myocardial and vascular level. In fact, numerous studies have shown that atherosclerosis is a process that lowers a highly significant inflammatory burden and that SGLT2i may have some role in inflammation. It is not possible to exclude that, considering the absence of the SGLT2 protein at the level of cardiomyocytes, SGLT2i may have an anti-atherosclerotic role through an anti-inflammatory action on endothelial cells.
In this special issue, concerning the relationships between SGLT2i and atherosclerosis, topics that address the relationships between the use of SGLT2i and the genesis and progression of atherosclerosis both at the vascular and at the myocardial level would be very well considered. Also important, clinical data that are able to substantiate an anti-atherosclerotic role of SGLT2i. For this reason, studies "in vitro" (on cells or organoids) or "in vivo" (on animals and humans) seem to be of great use, being able to generate data that would be very useful to the entire scientific community. However, epidemiological studies or meta-analyses could also contribute to the advancement of knowledge in this field. Finally, review articles could make it possible to make a State of Art and to understand what is currently the degree of scientific knowledge of the problem that is the subject of the special issue.
