myofibroblast의 조직손상시 wound healing에 관여하는 기능

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정상적인 muscle은 정적으로 서있는 상태에서 근수축을 하고 있을까?

-  아니다. 근수축은 거의 일어나지 않는다. 

resting tension이론, passive muscle stiffness이론에 의해 밝혀지고 있는 결과를 보면 거의 근수축을 안하고 있다. 

그렇다면 어떻게 passive muscle stiffness를 유지하여 인체가 정적인 자세로 있을때, 에너지 소비를 최소화하고 쉬게 할까?

1. Passive muscle stiffness may be influenced by active contractility of intramuscular connective tissue논문에 의하면 

"이 논문의 가설- perimysium(fascial layer) 근육내 결합조직은 active contraction을 할 수 있을 수 있고, passive muscle stiffness에 영향을 줄 수 있을 수 있음. 특히 tonic muscle에서"

myofibroblast

Location and function[edit]

Myofibroblasts are found subepithelially in many mucosal surfaces - for example, throughout almost the whole of the gastrointestinal and genitourinary tracts. Here they not only act as a regulator of the shape of the crypts and villi but also act as stem-niche cells in the intestinal crypts and as parts of atypical antigen presenting cells. They have both support as well as paracrine function in most places. In many organs like liver, lung, and kidney they are primarily involved in fibrosis. In the wound tissue they are implicated in wound strengthening by extracellular collagen fiber deposition and then wound contraction by intracellular contraction and concomitant alignment of the collagen fibers by integrin mediated pulling on to the collagen bundles. Pericytes and renal mesangial cells are some examples of modified myofibroblast like cells.

Myofibroblasts may interfere with the propagation of electrical signals controlling heart rhythm, leading to arrhythmia in both patients who have suffered a heart attack and in foetuses. Ursodiol is a promising drug for this condition.^[1]

Myofibroblasts in wound healing[edit]

Myofibroblasts can contract by using smooth muscle type actin-myosin complex, rich in a form of actin called alpha-smooth muscle actin. These cells are then capable of speeding wound repair by contracting the edges of the wound.

Early work on wound healing showed that granulation tissue taken from a wound could contract in vitro (or in an organ bath) in a similar fashion to smooth muscle, when exposed to substances that cause smooth muscle to contract, such as adrenaline or angiotensin.

More recently it has been shown that fibroblasts can transform into myofibroblasts with photobiomodulation.

After healing is complete, these cells are lost through apoptosis and it has been suggested that in several fibrotic diseases (for example liver cirrhosis, kidney fibrosis, retroperitoneal fibrosis) that this mechanism fails to work, leading to persistence of the myofibroblasts, and consequently expansion of the extracellular matrix (fibrosis) and contraction.

Similarly, in wounds that fail to resolve and become keloids or hypertrophic scars, myofibroblasts may persist, rather than disappearing by apoptosis.

그렇다면 결합조직이 심각하게 손상되는 pathology상황인 burn-scar contracture, breast-implant failure, abdominal adhesion strictures and Dupuytren’s disease에서는 어떤 일이 일어나는 것일까? 

그것에 관한 논문이다. 

During the past 20 years, it has become generally accepted that the modulation of fibroblastic cells towards the myofibroblastic phenotype, with acquisition of specialized contractile features, is essential for connective-tissue remodelling during normal and pathological wound healing. 

Yet the myofibroblast still remains one of the most enigmatic of cells, not least owing to its transient appearance in association with connective-tissue injury and to the difficulties in establishing its role in the production of tissue contracture. 

It is clear that our understanding of the myofibroblast — its origins, functions and molecular regulation — will have a profound influence on the future effectiveness not only of tissue engineering but also of regenerative medicine generally.

Myofibroblast와 조직손상시 결합조직의 mechanoreg.pdf

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