Chronic kidney disease (CKD) represents a major health problem worldwide, with an estimated prevalence of stages 1-4 of 16% in Europe and 13% in the US. Patients with end-stage kidney disease (ESKD) have an incredibly high risk of death and cardiovascular disease – risk which is not sufficiently explained by Framingham risk factors. For this reason, it appears tremendously challenging to be able to deepen the knowledge of the molecular mechanisms involved in CKD and its complications.
Whilst a proportion of the molecular mechanisms resulting in renal failure have already been unravelled, the precise molecular mechanisms underlining CKD complications have proven to be distinct and more complex. Such mechanisms are associated with coagulation abnormalities, endothelial dysfunction, vascular calcification, accumulation of uremic toxins, increased oxidative and metabolic stress and inflammation. As a further complication, a large proportion of CKD is due to the presence of other comorbidities, such as diabetes, hypertension or cardiovascular diseases. Even though several molecular mechanisms of nephropathy progression have been described, there is still a lacking of knowledge in this field. Understanding these mechanisms will potentially lead to the development of novel treatments able to slow the progression of the underlying CKD.
Finally, it is fundamental to consider that our knowledge of molecular mechanisms underlying CKD mainly derives from studies based on animal models and in vitro studies. Although essential for understanding the pathogenesis of CKD, their results may diverge from that obtained in real patients. In recent years, bioinformatics has emerged as a powerful tool for providing comprehensive insights into the molecular mechanisms of disease and identifying potential biomarkers and therapeutic targets. Novel methods, such as non-targeted high-resolution plasma proteome analysis, single-cell RNA sequencing and bioinformatics analyses applied to genome and proteome, might help in identifying novel, previously unelucidated pathways.
We invite researchers to contribute original research or review articles and we hope that this Research Topic will offer insight into the molecular mechanisms underpinning CKD. Articles may address the molecular mechanisms involved in the onset of CKD, as well as in the link between renal disease with other comorbidities or cardiovascular diseases. Potential topics include, but are not limited to, the following:
· Molecular mechanisms underlying onset and progression of CKD and/or ESRD
· Molecular mechanisms involved in cardiovascular and non-cardiovascular complications in CKD and/or ESRD
· Molecular mechanisms shared between kidney and other organs and/or diseases
· Recent discoveries in animal or in vitro models to unravel molecular mechanisms involved in CKD and/or ESRD
· New therapeutic strategies focused on molecular pathways in CKD/ESRD
· Novel methods to unravel molecular mechanisms involved in CKD, ESRD and their complications
Chronic kidney disease (CKD) represents a major health problem worldwide, with an estimated prevalence of stages 1-4 of 16% in Europe and 13% in the US. Patients with end-stage kidney disease (ESKD) have an incredibly high risk of death and cardiovascular disease – risk which is not sufficiently explained by Framingham risk factors. For this reason, it appears tremendously challenging to be able to deepen the knowledge of the molecular mechanisms involved in CKD and its complications.
Whilst a proportion of the molecular mechanisms resulting in renal failure have already been unravelled, the precise molecular mechanisms underlining CKD complications have proven to be distinct and more complex. Such mechanisms are associated with coagulation abnormalities, endothelial dysfunction, vascular calcification, accumulation of uremic toxins, increased oxidative and metabolic stress and inflammation. As a further complication, a large proportion of CKD is due to the presence of other comorbidities, such as diabetes, hypertension or cardiovascular diseases. Even though several molecular mechanisms of nephropathy progression have been described, there is still a lacking of knowledge in this field. Understanding these mechanisms will potentially lead to the development of novel treatments able to slow the progression of the underlying CKD.
Finally, it is fundamental to consider that our knowledge of molecular mechanisms underlying CKD mainly derives from studies based on animal models and in vitro studies. Although essential for understanding the pathogenesis of CKD, their results may diverge from that obtained in real patients. In recent years, bioinformatics has emerged as a powerful tool for providing comprehensive insights into the molecular mechanisms of disease and identifying potential biomarkers and therapeutic targets. Novel methods, such as non-targeted high-resolution plasma proteome analysis, single-cell RNA sequencing and bioinformatics analyses applied to genome and proteome, might help in identifying novel, previously unelucidated pathways.
We invite researchers to contribute original research or review articles and we hope that this Research Topic will offer insight into the molecular mechanisms underpinning CKD. Articles may address the molecular mechanisms involved in the onset of CKD, as well as in the link between renal disease with other comorbidities or cardiovascular diseases. Potential topics include, but are not limited to, the following:
· Molecular mechanisms underlying onset and progression of CKD and/or ESRD
· Molecular mechanisms involved in cardiovascular and non-cardiovascular complications in CKD and/or ESRD
· Molecular mechanisms shared between kidney and other organs and/or diseases
· Recent discoveries in animal or in vitro models to unravel molecular mechanisms involved in CKD and/or ESRD
· New therapeutic strategies focused on molecular pathways in CKD/ESRD
· Novel methods to unravel molecular mechanisms involved in CKD, ESRD and their complications