Skeletal muscle (SM) comprises around 40% of total body weight and is among the most important plastic tissues, as it supports skeletal development, controls body temperature, and manages glucose levels. Extracellular matrix (ECM) maintains the integrity of SM, enables biochemical signaling, provides structural support, and plays a vital role during myogenesis. Several human diseases are coupled with dysfunctions of the ECM, and several ECM components are involved in disease pathologies that affect almost all organ systems. Thus, mutations in ECM genes that encode proteins and their transmembrane receptors can result in diverse SM diseases, a large proportion of which are types of fibrosis and muscular dystrophy. In this review, we present major ECM components of SMs related to muscle-associated diseases and discuss two major ECM myopathies, namely, collagen myopathy and laminin myopathies, and their therapeutic management. A comprehensive understanding of the mechanisms underlying these ECM-related myopathies would undoubtedly aid the discovery of novel treatments for these devastating diseases.
I'm super interested but not particularly well read in mycorrhizal interactions but I've never seen findings like these before and my cellular microbiology and o-chem knowledge is extremely lacking, but I dont understans how this differs from "GMO" with a retrovirus or interspecific extra cellular vesicles.
I'd also be happy with articles to read if there's not an easy answer for tgis, i'm just wondering what this phenomenon is called and how normal it is expected to be.
In human development, ECM is laid down, and that which isn't turned over accumulates damage such as crosslinks (AGEs) or breakdown of components (elastin), leading to stiff arteries and weak skin, and affecting cell behavior.
This process takes decades in humans, and I assume it's driven by spontaneous chemical reactions, not some biological clock, so it seems like it should happen at the same speed across species with similar ECMs. Does it? This would cause short-lived animals to die with good ECM and long-lived animals to die with very damaged ECM. Alternatively, does the rate of damage adjust to the species lifespan, and if so, how?
A recent publication (El-Shennawy et al 2022) suggests that people infected with SARS-CoV-2 release extracellular vesicles (EVs) that have the ACE2 receptor on their membranes, acting as a decoy for the virus to infect instead of cells.
Has this been seen in any other viral diseases? I've never heard of this before, not sure if it even falls under the "immune system" label or not.
Maybe decoy vesicles with receptors targeted by viruses are going to be produced as antivirals?
The Guyton and Hall Textbook of Medical Physiology, p. 76, says: > For example, a high extracellular fluid calcium ion concentration decreases membrane permeability to sodium ions and simultaneously reduces excitability.
Why does this hold?
Naively, a high extracellular concentration of calcium ions should facilitate their flow through the calcium channels. Since the flow contributes to the action potential, the neurons should actually become hyperexcitable in the such a situation.
Is it possibly the case that a high extracellular concentration of calcium increases the extracellular potential, thus causing hyperpolarization of the cell? This doesn't make too much sense either because, then, a high extracellular concentration of Na+ would also decrease the excitability in a similar way.
https://preview.redd.it/pdtfm0tevxa81.jpg?width=685&format=pjpg&auto=webp&s=b2c5410a57d7feb18ff369fa6451c0928b9db335
Hi! I don't get why increased extracellular potassium does not lead to an action potential? I know that the resting potential is decreasing due to this variation but I don't know if or how it is linked to it ? Thank you in advance!
A recent publication (El-Shennawy et al 2022) suggests that people infected with SARS-CoV-2 release extracellular vesicles (EVs) that have the ACE2 receptor on their membranes, acting as a decoy for the virus to infect instead of cells.
Has this been seen in any other viral diseases? I've never heard of this before, not sure if it even falls under the "immune system" label or not.
Maybe decoy vesicles with receptors targeted by viruses are going to be produced as antivirals?
