TRPM7: Difference between revisions
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*'''[[Diabetes (TRPM7)]]''' | *'''[[Diabetes (TRPM7)]]''' | ||
*'''[[Nephrology clinical (TRPM7)]]''' | *'''[[Nephrology clinical (TRPM7)]]''' | ||
*'''[[Nephrology experimental (TRPM7)]]''' | |||
*'''[[Fibrosis (TRPM7)]]''' | *'''[[Fibrosis (TRPM7)]]''' | ||
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*'''[[Cancer (TRPM7)]]''' | *'''[[Cancer (TRPM7)]]''' | ||
*'''[[Structure Signal Transduction]]''' | *'''[[Structure Signal Transduction]]''' | ||
*'''[[RNA (TRMP7)]]''' | |||
*'''[[Cell Death (TRPM7)]]''' | *'''[[Cell Death (TRPM7)]]''' | ||
*'''[[Toxic cations (TRPM7)]]''' | *'''[[Toxic cations (TRPM7)]]''' | ||
| Line 22: | Line 24: | ||
*'''[[Immunology (TRPM7)]]''' | *'''[[Immunology (TRPM7)]]''' | ||
*'''[[Pharmacology (TRPM7)]]''' | *'''[[Pharmacology (TRPM7)]]''' | ||
*'''[[ | *'''[[Drug-induced Hypomagnesemia (TRPM7)]]''' | ||
*'''[[Human genetics (TRPM7)]]''' | *'''[[Human genetics (TRPM7)]]''' | ||
*'''[[Magnesium renal (TRPM7)]]''' | |||
*'''[[Magnesium intestinal (TRPM7)]]''' | |||
*'''[[Magnesium physiology (TRPM7)]]''' | *'''[[Magnesium physiology (TRPM7)]]''' | ||
*'''[[Off-topic papers found while searching (TRPM7)]]''' | *'''[[Off-topic papers found while searching (TRPM7)]]''' | ||
*'''[[Reviews and multitopic]]''' | |||
*'''[[Lung (TRPM7)]]''' | |||
*'''[[Heart (TRPM7)]]''' | |||
*'''[[Muscle (TRPM7)]]''' | |||
*'''[[Liver (TRPM7)]]''' | |||
*'''[[Thyroid (TRPM7)]]''' | |||
*'''[[Cajal cells (TRPM7)]]''' | |||
*'''[[Development (TRPM7)]]''' | |||
*'''[[Analytical Methods (TRPM7)]]''' | |||
*'''[[]]''' | *'''[[]]''' | ||
*'''[[]]'' | *'' '''[[Magnesium Channels and Modulators]]''' '' | ||
Latest revision as of 11:33, 27 January 2024
TRPM7 as member or the Transient Receptor Potential Ion Channel family is a nonselective cation channel which is inhibited by magnesium. It imports toxic cations like Zn2+, Cd2+, Co2+, and its kinase function hase some specific effects. Activity is needed for cellular magnesium import. Essential for Fibrosis (EMT), Calcification processes, Cell viability, it transforms magnesium action into cardiovascular, renal and neurologic diseases. While clinical trial data on magnesium substitution is lacking, physiological effects of established leads as sacubitril, candesartan, and aldosterone antagonism act as TRPM7 inhibitors.
Actual PubMed searches run with [www.moremed.org/sitesearch.php] will be sorted into these topical collections:
- Bone and Implants (TRPM7)
- Vascular Calcification (TRPM7)
- Hypertension
- Glomus caroticus
- Diabetes (TRPM7)
- Nephrology clinical (TRPM7)
- Nephrology experimental (TRPM7)
- Fibrosis (TRPM7)
- Neurology (TRPM7)
- Cancer (TRPM7)
- Structure Signal Transduction
- RNA (TRMP7)
- Cell Death (TRPM7)
- Toxic cations (TRPM7)
- Myalgic encephalitis
- Coronaviruses (TRPM7)
- Sepsis Coagulation AKI
- Immunology (TRPM7)
- Pharmacology (TRPM7)
- Drug-induced Hypomagnesemia (TRPM7)
- Human genetics (TRPM7)
- Magnesium renal (TRPM7)
- Magnesium intestinal (TRPM7)
- Magnesium physiology (TRPM7)
- Off-topic papers found while searching (TRPM7)
- Reviews and multitopic
- Lung (TRPM7)
- Heart (TRPM7)
- Muscle (TRPM7)
- Liver (TRPM7)
- Thyroid (TRPM7)
- Cajal cells (TRPM7)
- Development (TRPM7)
- Analytical Methods (TRPM7)
- [[]]
- Magnesium Channels and Modulators