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Posted On: 12/25/2022 5:49:04 PM
Post# of 148878
Re: chazzledazzle #131957
Adding one EDS paper…EDS largely seems to me to be genetic, but I’m still wondering about LL ability to tamp down the inflammatory and immune modulation after effects of the previously cast die.
“ECM components also modulate immune cell migration into inflamed tissues and their activation and proliferation [23]. The stimulation of the innate immunity results from the recognition of specific mediators, namely pattern recognition receptors, which, in turn, recognize molecules, referred as danger-associated molecular patterns, which are released from damaged tissues [24]. It is well documented that different ECM components or their fragments including the fibronectin 1 extra domain A, one of the alternative spliced regions of fibronectin encoding gene, tenascin-C, fibrinogen, and several proteoglycans, serve as danger signals and trigger immune responses following tissue damage or in response to pathological ECM remodeling [24,25]. In fibrotic conditions, increased ECM production, accumulation of ECM fragments, augmented secretion of cytokines, fibroblast-to-myofibroblast transition, and activation of immune responses, dependent on toll-like receptors, occur [26]. The regulation of ECM synthesis and remodeling is central for human health, as recognized in different heritable connective tissue disorders [1,27]. Indeed, molecular defects in a large range of ECM-related genes, including those encoding enzymes involved in biosynthesis or processing of ECM proteins, cause a myriad of connective tissue disorders, e.g., Ehlers–Danlos syndromes, Osteogenesis imperfecta, Marfan syndrome, Loeys–Dietz syndromes, arterial tortuosity syndrome, and numerous skeletal dysplasias [1,27]. These disorders are characterized by a multisystem involvement in terms of cardiovascular, skeletal, and cutaneous features [28], highlighting the functional relevance of the ECM in ensuring the integrity and function of several connective tissues.
The pathological consequences of defects in ECM components depend on the balance between extracellular effects, e.g., reduced protein secretion and export of misfolded proteins, and intracellular consequences such as apoptosis activation, ER dysfunction, and autophagy perturbation that impact in different ways on the molecular pathology and disease severity [27,29,30,31].”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723307/
Like I said before, I find it fun to think about.
“ECM components also modulate immune cell migration into inflamed tissues and their activation and proliferation [23]. The stimulation of the innate immunity results from the recognition of specific mediators, namely pattern recognition receptors, which, in turn, recognize molecules, referred as danger-associated molecular patterns, which are released from damaged tissues [24]. It is well documented that different ECM components or their fragments including the fibronectin 1 extra domain A, one of the alternative spliced regions of fibronectin encoding gene, tenascin-C, fibrinogen, and several proteoglycans, serve as danger signals and trigger immune responses following tissue damage or in response to pathological ECM remodeling [24,25]. In fibrotic conditions, increased ECM production, accumulation of ECM fragments, augmented secretion of cytokines, fibroblast-to-myofibroblast transition, and activation of immune responses, dependent on toll-like receptors, occur [26]. The regulation of ECM synthesis and remodeling is central for human health, as recognized in different heritable connective tissue disorders [1,27]. Indeed, molecular defects in a large range of ECM-related genes, including those encoding enzymes involved in biosynthesis or processing of ECM proteins, cause a myriad of connective tissue disorders, e.g., Ehlers–Danlos syndromes, Osteogenesis imperfecta, Marfan syndrome, Loeys–Dietz syndromes, arterial tortuosity syndrome, and numerous skeletal dysplasias [1,27]. These disorders are characterized by a multisystem involvement in terms of cardiovascular, skeletal, and cutaneous features [28], highlighting the functional relevance of the ECM in ensuring the integrity and function of several connective tissues.
The pathological consequences of defects in ECM components depend on the balance between extracellular effects, e.g., reduced protein secretion and export of misfolded proteins, and intracellular consequences such as apoptosis activation, ER dysfunction, and autophagy perturbation that impact in different ways on the molecular pathology and disease severity [27,29,30,31].”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723307/
Like I said before, I find it fun to think about.
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