Adequate intake of various minerals over the life of an organism is essential to the prevention of several chronic, long-latency diseases (e.g., certain common cancers [colon, Breast], cardiovascular disease, metabolic diseases [diabetes and non-alcoholic fatty liver disease], osteoporosis, chronic kidney disease, early-onset dementia and various skin diseases). Chronic inflammation is a consistent intermediate. The cellular and molecular events that work to prevent chronic diseases from developing (and progressing) depend on appropriate levels of the same trace elements. Which individual minerals are critical and how they function to modify critical cellular and molecular pathways is not completely understood? Among cationic elements, calcium stands alone as a universal first- and second-messenger; it is critical to virtually every biological process. Beyond calcium is a group of cationic elements including copper, cobalt, chromium, iron, magnesium, manganese, selenium and zinc and others. Like calcium, these elements are known to play critical roles in multiple biological processes. Like calcium, these elements have recommended daily intake levels. Deficiencies of these minerals and trace elements are known to occur and are associated with disease states. Further down the line are the trace elements (e.g., lanthanides, actinides and others) that are utilized in such small amounts that we do not know for certain whether deficiencies do, in fact, exist. Which cellular / molecular processes are negatively-impacted by a lack of one or more trace elements is also not known in many cases as are the possible relationships to chronic disease states.
This theme-issue hopes to attract manuscripts of all types (original research articles, reports of original clinical and epidemiological research, review articles and short commentaries) that address the role of specific individual mineral or trace elements or multiple elements working together in the regulation of cellular and molecular processes. The ultimate goal is to help unravel mechanisms that connect trace element deficiencies to initiation and progression of chronic, long-latency diseases.
It is well-known, of course, that exposure to high levels of certain trace elements is disease-producing. While many of the pathophysiological events that lead to acute toxicity are understood, the relationship between sub-acute toxicities and alterations in important cellular and molecular processes is unclear. How such sub-acute toxicities impact chronic, long-latency diseases is even less clear. Manuscripts that address these issues are also welcome.
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Adequate intake of various minerals over the life of an organism is essential to the prevention of several chronic, long-latency diseases (e.g., certain common cancers [colon, Breast], cardiovascular disease, metabolic diseases [diabetes and non-alcoholic fatty liver disease], osteoporosis, chronic kidney disease, early-onset dementia and various skin diseases). Chronic inflammation is a consistent intermediate. The cellular and molecular events that work to prevent chronic diseases from developing (and progressing) depend on appropriate levels of the same trace elements. Which individual minerals are critical and how they function to modify critical cellular and molecular pathways is not completely understood? Among cationic elements, calcium stands alone as a universal first- and second-messenger; it is critical to virtually every biological process. Beyond calcium is a group of cationic elements including copper, cobalt, chromium, iron, magnesium, manganese, selenium and zinc and others. Like calcium, these elements are known to play critical roles in multiple biological processes. Like calcium, these elements have recommended daily intake levels. Deficiencies of these minerals and trace elements are known to occur and are associated with disease states. Further down the line are the trace elements (e.g., lanthanides, actinides and others) that are utilized in such small amounts that we do not know for certain whether deficiencies do, in fact, exist. Which cellular / molecular processes are negatively-impacted by a lack of one or more trace elements is also not known in many cases as are the possible relationships to chronic disease states.
This theme-issue hopes to attract manuscripts of all types (original research articles, reports of original clinical and epidemiological research, review articles and short commentaries) that address the role of specific individual mineral or trace elements or multiple elements working together in the regulation of cellular and molecular processes. The ultimate goal is to help unravel mechanisms that connect trace element deficiencies to initiation and progression of chronic, long-latency diseases.
It is well-known, of course, that exposure to high levels of certain trace elements is disease-producing. While many of the pathophysiological events that lead to acute toxicity are understood, the relationship between sub-acute toxicities and alterations in important cellular and molecular processes is unclear. How such sub-acute toxicities impact chronic, long-latency diseases is even less clear. Manuscripts that address these issues are also welcome.
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.