Mineral ion homeostasis is essential for maintaining proper biological functions and activities in cells, tissues, and organs. For years, the physiological roles and interplays of mineral regulatory hormones - fibroblast growth factor 23 (FGF23) with its co-receptor Klotho, parathyroid hormone (PTH), and vitamin D - and their feedback loop have been studied in kidneys, parathyroid glands, bones, and intestine. These hormones are also known to have extra-mineral actions, so that their pathological alterations may lead to either mineral or non-mineral imbalances. In turn, these affect multiple vital systems or functions such as bone mineralization, cardiovascular health, erythropoiesis, and immunity.
The advances in next-generation sequencing (NGS) technologies and genome-wide association studies (GWAS) have rapidly progressed, thereby massively expanding our understanding of biological and pathological processes. There is an increased focus on epigenetic regulations and RNA modifications, also in the field of mineral metabolism.
It is very important to build new evidence of the pathophysiological mechanisms focusing on the regulations and interplays among mineral regulatory hormones, including FGF23/Klotho, PTH, and vitamin D, via integrating new findings from various aspects including genetic and epigenetic mechanisms.
This issue focuses on new mechanisms of mineral ion regulation that expand on previous research from genetic, epigenetic (DNA methylation, histone modification, non-coding RNA, and RNA modification), and post-translational aspects, all of which are emerging as new potential regulators of mineral metabolism. These new regulators might contribute to various pathogenetic processes. We also welcome to submit other research areas regarding mineral metabolism regulation.
This research topic will provide new insights into endocrine regulation of mineral ion homeostasis from a wide range of research areas with various approaches, which leads to identifying potential new therapeutic targets and agents of mineral imbalance and related diseases.
Mineral ion homeostasis is essential for maintaining proper biological functions and activities in cells, tissues, and organs. For years, the physiological roles and interplays of mineral regulatory hormones - fibroblast growth factor 23 (FGF23) with its co-receptor Klotho, parathyroid hormone (PTH), and vitamin D - and their feedback loop have been studied in kidneys, parathyroid glands, bones, and intestine. These hormones are also known to have extra-mineral actions, so that their pathological alterations may lead to either mineral or non-mineral imbalances. In turn, these affect multiple vital systems or functions such as bone mineralization, cardiovascular health, erythropoiesis, and immunity.
The advances in next-generation sequencing (NGS) technologies and genome-wide association studies (GWAS) have rapidly progressed, thereby massively expanding our understanding of biological and pathological processes. There is an increased focus on epigenetic regulations and RNA modifications, also in the field of mineral metabolism.
It is very important to build new evidence of the pathophysiological mechanisms focusing on the regulations and interplays among mineral regulatory hormones, including FGF23/Klotho, PTH, and vitamin D, via integrating new findings from various aspects including genetic and epigenetic mechanisms.
This issue focuses on new mechanisms of mineral ion regulation that expand on previous research from genetic, epigenetic (DNA methylation, histone modification, non-coding RNA, and RNA modification), and post-translational aspects, all of which are emerging as new potential regulators of mineral metabolism. These new regulators might contribute to various pathogenetic processes. We also welcome to submit other research areas regarding mineral metabolism regulation.
This research topic will provide new insights into endocrine regulation of mineral ion homeostasis from a wide range of research areas with various approaches, which leads to identifying potential new therapeutic targets and agents of mineral imbalance and related diseases.
