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10.1016/j.biomaterials.2023.122340 http://scihub22266oqcxt.onion/10.1016/j.biomaterials.2023.122340 37774552!?!37774552 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=37774552&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Biomaterials 2023 ; 302 (?): 122340 Nephropedia Template TP {{tp|p=37774552|t=2023. Calcium carbonate-actuated ion homeostasis perturbator for oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy |pdf=|usr=}}{{37774552}} gab.com Text Calcium carbonate-actuated ion homeostasis perturbator for oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy JO: Biomaterials http://www.kidney.de/pget.php?&tw=1&pmid=37774552 #FOAvip Ion homeostasis distortion through exogenous overload or underload of intracellular ion species has become an arresting therapeutic approach against malignant tumor. Nevertheless, treatment outcomes of such ion interference are always compromised by the intrinsic ion homeostasis maintenance systems in cancer cells. Herein, an ion homeostasis perturbator (CTC) is facilely designed by co-encapsulation of carvacrol (CAR) and meso-tetra-(4-carboxyphenyl)porphine (TCPP) into pH-sensitive nano-CaCO(3), aiming to disrupt the self-defense mechanism during the process of ion imbalance. Upon the endocytosis of CTC into tumor cells, lysosomal acidity can render the decomposition of CaCO(3), resulting in the instant Ca(2+) overload and CO(2) generation in cytoplasm. Simultaneously, CaCO(3) disintegration triggers the release of CAR and TCPP, which are devoted to TRPM7 inhibition and sonosensitization, respectively. The malfunction of TRPM7 can impede the influx of Mg(2+) and allow unrestricted influx of Ca(2+) based on the antagonism relationship between Mg(2+) and Ca(2+), leading to an aggravated Ca(2+)/Mg(2+) dyshomeostasis through ion channel deactivation. In another aspect, US-triggered cavitation can be significantly enhanced by the presence of inert CO(2) microbubbles, further amplifying the generation of reactive oxygen species. Such oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy effectively impairs the mitochondrial function of tumor, which may provide useful insights in cancer therapy. Twit Text FOAVip Calcium carbonate-actuated ion homeostasis perturbator for oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy ????Biomaterials http://www.kidney.de/pget.php?&tw=1&pmid=37774552 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=37774552 #FOAvip English Wikipedia <ref>{{Cite pmid|37774552}}</ref> Calcium carbonate-actuated ion homeostasis perturbator for oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy #MMPMID37774552 Huang J; He J; Wang J; Li Y; Xu Z; Zhang L; Kang Y; Xue P Biomaterials 2023[Nov]; 302 (?): 122340 PMID37774552show ga Ion homeostasis distortion through exogenous overload or underload of intracellular ion species has become an arresting therapeutic approach against malignant tumor. Nevertheless, treatment outcomes of such ion interference are always compromised by the intrinsic ion homeostasis maintenance systems in cancer cells. Herein, an ion homeostasis perturbator (CTC) is facilely designed by co-encapsulation of carvacrol (CAR) and meso-tetra-(4-carboxyphenyl)porphine (TCPP) into pH-sensitive nano-CaCO(3), aiming to disrupt the self-defense mechanism during the process of ion imbalance. Upon the endocytosis of CTC into tumor cells, lysosomal acidity can render the decomposition of CaCO(3), resulting in the instant Ca(2+) overload and CO(2) generation in cytoplasm. Simultaneously, CaCO(3) disintegration triggers the release of CAR and TCPP, which are devoted to TRPM7 inhibition and sonosensitization, respectively. The malfunction of TRPM7 can impede the influx of Mg(2+) and allow unrestricted influx of Ca(2+) based on the antagonism relationship between Mg(2+) and Ca(2+), leading to an aggravated Ca(2+)/Mg(2+) dyshomeostasis through ion channel deactivation. In another aspect, US-triggered cavitation can be significantly enhanced by the presence of inert CO(2) microbubbles, further amplifying the generation of reactive oxygen species. Such oxidative damage-augmented Ca(2+)/Mg(2+) interference therapy effectively impairs the mitochondrial function of tumor, which may provide useful insights in cancer therapy. |*TRPM Cation Channels[MESH] |Calcium Carbonate[MESH] |Calcium/metabolism[MESH] |Carbon Dioxide[MESH] |Homeostasis[MESH] |Oxidative Stress[MESH]Calcium carbonate-actuated ion homeostasis perturbator for oxidative (epmc).pdf DeepDyve Pubget Overpricing