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10.1016/j.jhep.2021.01.043 http://scihub22266oqcxt.onion/10.1016/j.jhep.2021.01.043 33571553!8217299!33571553     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Hepatol 2021 ; 75 (1): 34-45 Nephropedia Template TP {{tp|p=33571553|t=2021. Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH |pdf=|usr=}}{{33571553}} gab.com Text Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH JO: J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=33571553 #FOAvip BACKGROUND & AIMS: Perturbations of intracellular magnesium (Mg(2+)) homeostasis have implications for cell physiology. The cyclin M family, CNNM, perform key functions in the transport of Mg(2+) across cell membranes. Herein, we aimed to elucidate the role of CNNM4 in the development of non-alcoholic steatohepatitis (NASH). METHODS: Serum Mg(2+) levels and hepatic CNNM4 expression were characterised in clinical samples. Primary hepatocytes were cultured under methionine and choline deprivation. A 0.1% methionine and choline-deficient diet, or a choline-deficient high-fat diet were used to induce NASH in our in vivo rodent models. Cnnm4 was silenced using siRNA, in vitro with DharmaFECT and in vivo with Invivofectamine(R) or conjugated to N-acetylgalactosamine. RESULTS: Patients with NASH showed hepatic CNNM4 overexpression and dysregulated Mg(2+) levels in the serum. Cnnm4 silencing ameliorated hepatic lipid accumulation, inflammation and fibrosis in the rodent NASH models. Mechanistically, CNNM4 knockdown in hepatocytes induced cellular Mg(2+) accumulation, reduced endoplasmic reticulum stress, and increased microsomal triglyceride transfer activity, which promoted hepatic lipid clearance by increasing the secretion of VLDLs. CONCLUSIONS: CNNM4 is overexpressed in patients with NASH and is responsible for dysregulated Mg(2+) transport. Hepatic CNNM4 is a promising therapeutic target for the treatment of NASH. LAY SUMMARY: Cyclin M4 (CNNM4) is overexpressed in non-alcoholic steatohepatitis (NASH) and promotes the export of magnesium from the liver. The liver-specific silencing of Cnnm4 ameliorates NASH by reducing endoplasmic reticulum stress and promoting the activity of microsomal triglyceride transfer protein. Twit Text FOAVip Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH ????J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=33571553 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33571553 #FOAvip English Wikipedia <ref>{{Cite pmid|33571553}}</ref> Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH #MMPMID33571553 Simon J; Goikoetxea-Usandizaga N; Serrano-Macia M; Fernandez-Ramos D; Saenz de Urturi D; Gruskos JJ; Fernandez-Tussy P; Lachiondo-Ortega S; Gonzalez-Recio I; Rodriguez-Agudo R; Gutierrez-de-Juan V; Rodriguez-Iruretagoyena B; Varela-Rey M; Gimenez-Mascarell P; Mercado-Gomez M; Gomez-Santos B; Fernandez-Rodriguez C; Lopitz-Otsoa F; Bizkarguenaga M; Dames S; Schaeper U; Martin F; Sabio G; Iruzubieta P; Crespo J; Aspichueta P; Chu KH; Buccella D; Martin C; Delgado TC; Martinez-Cruz LA; Martinez-Chantar ML J Hepatol 2021[Jul]; 75 (1): 34-45 PMID33571553show ga BACKGROUND & AIMS: Perturbations of intracellular magnesium (Mg(2+)) homeostasis have implications for cell physiology. The cyclin M family, CNNM, perform key functions in the transport of Mg(2+) across cell membranes. Herein, we aimed to elucidate the role of CNNM4 in the development of non-alcoholic steatohepatitis (NASH). METHODS: Serum Mg(2+) levels and hepatic CNNM4 expression were characterised in clinical samples. Primary hepatocytes were cultured under methionine and choline deprivation. A 0.1% methionine and choline-deficient diet, or a choline-deficient high-fat diet were used to induce NASH in our in vivo rodent models. Cnnm4 was silenced using siRNA, in vitro with DharmaFECT and in vivo with Invivofectamine(R) or conjugated to N-acetylgalactosamine. RESULTS: Patients with NASH showed hepatic CNNM4 overexpression and dysregulated Mg(2+) levels in the serum. Cnnm4 silencing ameliorated hepatic lipid accumulation, inflammation and fibrosis in the rodent NASH models. Mechanistically, CNNM4 knockdown in hepatocytes induced cellular Mg(2+) accumulation, reduced endoplasmic reticulum stress, and increased microsomal triglyceride transfer activity, which promoted hepatic lipid clearance by increasing the secretion of VLDLs. CONCLUSIONS: CNNM4 is overexpressed in patients with NASH and is responsible for dysregulated Mg(2+) transport. Hepatic CNNM4 is a promising therapeutic target for the treatment of NASH. LAY SUMMARY: Cyclin M4 (CNNM4) is overexpressed in non-alcoholic steatohepatitis (NASH) and promotes the export of magnesium from the liver. The liver-specific silencing of Cnnm4 ameliorates NASH by reducing endoplasmic reticulum stress and promoting the activity of microsomal triglyceride transfer protein. |*Magnesium/blood/metabolism[MESH] |*Non-alcoholic Fatty Liver Disease/metabolism/pathology[MESH] |Animals[MESH] |Biological Transport/drug effects[MESH] |Carrier Proteins/*metabolism[MESH] |Cation Transport Proteins/*metabolism[MESH] |Cells, Cultured[MESH] |Disease Models, Animal[MESH] |Drug Discovery[MESH] |Endoplasmic Reticulum Stress/drug effects[MESH] |Gene Expression Regulation[MESH] |Hepatocytes/*metabolism[MESH] |Humans[MESH]Magnesium accumulation upon cyclin M4 silencing activates microsomal t(epmc).pdf DeepDyve Pubget Overpricing