The sequentially broken capillary cell dance, with its diminished alternating flux of outer membrane permeability and the back and forth swinging of mitochondrial combustion between energy and nitric oxide gas, becomes the reverberating signaling linchpin within the cell that disrupts its counterbalancing homeostasis and dance step multipurpose 5,6,7. The reverberation will pace a similar signaling disarray of rhythm streams into its interstitial space and its end organ cellular domain 6,7. The dance tailspin will eventually trigger such a sustained drop in counterbalancing nitric oxide combustion that reburbishment of its infrastructure becomes critically muted. As capillary cell mitochondrial volumes and mass decrease and its outer membrane complex pseudocapillarizes, immune choreogaphy mistakes funneled into the interstitial space mount.

The newly funneled interstitial space immune designees become increasingly misaligned and misappropriated to the original but now blurred capillary cell choreography intent of eliminating the cadre of vascular inflammatory free radical displays harbored there 6,7. Instead, these wayward immune arsenal contingents can be signal manipulated or turned by rogue signaling streams to execute a divergent purpose that could run counter to eliminating vascular inflammatory free radicals. As these increasingly divergent interstitial space signaling streams gain traction, they can colink their rhythm patterns to remaster the interstitial space signaling apparatus and further erode what was once a dominant anti-inflammatory rhythm invoked from immune arsenal displays that were choreograhed from a counterbalancing and healthy capillary cell pivot and swing dance step rhythm 6,7. 

As upstream end organ capillary and downstream endothelial cell mitochondria become increasingly preoccupied with energy combustion, due to the increasing inability to eliminate interstitial space inflammatory breach, the loss of the sequential pivot and swing dance step rhythm will serially usurp the cell’s capacity to manage its interlocking and dance step counterbalancing signal loops 6,7. The loss of counterbalance and infrastructure signaling homeostasis will affect all of its infrastrucrue and how and what its organelles will signal respond to. As counterbalance is lost within the cell, it will signal cascade alternative and overly redundant rhythms that create further signaling snafus that cannot be adequately counterbalanced as the loss of dance step rhythm has canceled out much needed refurbishment of over utilized switches, enzymes, and other displays while overutilizing other systems that exhaust antioxidants and increase certain free radicals 7.

An obvious example of toxic overproduction from the lost dance step rhythm is the mitochondrial generated ROS combustion exhaust from excessive energy combustion 5,6,7. Under optimal signaling homeostasis and counterbalancing dance step rhythm, reactive oxygen species generated form the mitochondrial oxygen combustion cycle is an important attachment cog in the overall capillary cell outer membrane scheme of expanding a precision based immune arsenal funneling into the interstitial space in order to timely eliminate inflammatory breach. This ROS assisted immune arsenal expansion into the interstitial space will enable a successful inflammatory breach removal which pushes an interstitial space all clear signal that will induce a capillary cell permeablity contraction of immune arsenal displays and subsequent timely swing of combustion to nitric oxide. The sequential generation of ROS exhaust in the setting of a capillary cell dance step rhythm assists in a precision based expansion of interstitial space inflammatory mediators that makes it more likely to remove inflammatory breach in a timely manner to allow the next signal counterbalancing dance step 7. 

When the sequential capillary cell dance step rhythm is misaligned or not sufficiently counterbalanced, such that there is excessive mitochondrial energy combustion and too much ROS exhaust, the rhythm and purpose of ROS attachments in the context of it being part of an anti-inflammatory rhythm is lost 7. Instead the excessive ROS will not be effectively controlled by intercellular counterbalancing rhythm displays that would limit its combustion production and the supply of oxidants required to neutralize it. As a result, its levels within the cell will increase that will create opportunity for erroneous ROS attachments that could damage, silence or change purpose of various membrane surfaces and nuclear chromosomal DNA that it was not originally intended to do. These attachments will further cascade aberrant and unbalanced intercellular signaling rhythms which make the cell and interstitial space vulnerable to additional chronic proinflammatory signaling rhythm streams in what becomes a self perpetuating cascade. The persistent ROS aberrant membrane attachment surge, will contribute to intercellular signaling rhythm imbalances that will bias increases in gluconeogenesis fermentation (over glycolysis), shift substrate utilization (fatty acids over pyruvate) that produces mitochondrial acetyl CoA and then where it is utilized (Krebs cycle over ribosomes) and how other cytoplasmic organelles such as liposomes (lipid peroxidation over lipogenesis) or ribosomes and rough endoplasmic reticulum will function or stay dormant 7.  

The ROS signaling switch is just one example of how the lack of counterbalancing from the loss of a sequential dance step rhythm can cause capillary cell signaling infrastructure to run amok. The loss of dance step rhythm, and the subsequent underproduction of nitric oxide produced RNS exhaust, could have the same detrimental effect on infrastructure refurbishment and other purposes of nitric oxide combustion as too much ROS would have in the execution of purpose in the energy combustion cycle. As might be expected the lack of counterbalanced signaling influences within the capillary cell, of either too much energy combustion and excessive ROS or too little nitric oxide combustion and too little RNS, will have adverse signaling consequences to the maintenance and longevity of its cellular homeostasis, its capacity to manage interstitial space hygiene and respond to end organ functional requirements7. The sequential capillary and downstream endothelial cell decline in signaling purpose not only involves its infrastructure and the decay of its outer membrane complex, but will extend to involve the operations of its interstitial space domain and how its interacts with circulating red and white blood cells, immunoglboulins, platelets, clotting factors, complement, albumen and inflammatory proteins6.

As the capillary cell dance step rhythm deteriorates and the execution of its multipurpose weakens, it becomes increasingly incapable of signal pacing and leading interstitial space anti-inflammatory rhythm streams. This will enable an increase in signaling mistakes towards the timely removal of inflammatory breach, a sequential loss of refurbishment to its infrastructure (or that of its allied cells) and an increasing inability to optimally respond to end organ functional requirements. Most important it will contribute to the increasing displays of organizing chronic inflammatory signaling rhythms from turned immune arsenal and mesenchymal cells that will introduce end organ interstitial space disease consortiums.