Unsticking Your Fascia: Why Your Body’s Hidden Waterways Get Stuck……

Meet hyaluronan — the “behind-the-scenes” molecule deciding whether your tissues glide like silk or seize like a rusted hinge

Part 1 of a four-article series by Dr Karen Kirkness

A river system running beneath your skin

Underneath your skin, wrapped around every muscle, vessel and organ, runs a body-wide network most people never learn the name of: fascia. It is often described as a bag holding you together, but that undersells it badly. A better image is a river system. The interstitium is just that; a continuous, branching network of fluid-filled planes that is supposed to let your tissues ease past one another every time you reach, twist, breathe or walk. 

When those waterways run clear, movement is close to effortless. When they silt up, tissue planes that used to glide start to catch, like drawers swollen shut after a humid summer. This series is about that silting-up process — what actually causes it at a molecular level, and what the evidence says you can do about it.

What fascia and hyaluronan actually are

Strip away the metaphor and fascia is a specialised connective tissue with both fibrous and gel-like components, the gel portion built largely from a molecule called hyaluronan, or HA. HA is an ancient molecule, found across bacteria and vertebrates alike. It has one extraordinary physical property that explains almost everything else about it: its domain holds roughly a thousand times its own weight in water. 

A small amount of HA in your fascia creates a large amount of hydration, viscosity and cushioning, which is exactly why the amount and molecular weight of HA in a given fascial interface correlates with how much gliding and mechanical function the region actually needs.

Fasciacytes: cells devoted to keeping the water moving

This hydration isn’t accidental or passive. Fascia contains a specialised population of cells called fasciacytes, distinct from ordinary fibroblasts, whose defining feature is unusually high expression of the enzyme HAS2 — the machinery that builds HA (Stecco et al., 2018). 

HAS2 has been described as functioning like a biological 3D printer: it builds the HA polymer chain on one side of the cell membrane while threading it directly out into the tissue on the other, manufacturing and delivering the product in a single continuous process. Fasciacytes, essentially, keep your fascial waterways plumped and hydrated. 

The effect is often likened to lubrication; although this mischaracterizes the relationship somewhat, as the relationship isn’t a mechanical one in the sense of oiling metal parts to get them sliding (Sharkey & Kirkness, 2025). Hydration allows for what we may think of as viscoelastic buffering, whereby the networked volumes can glide freely along the “hydration-plumped” interfaces. 

The CHA axis: how tissue feels load and answers with fluid

The genuinely elegant part is how this system “knows” when to produce more. My co-authored review proposes what we call the Calcium–Hyaluronan (CHA) axis: mechanical stress on fascia opens calcium channels — Piezo1, TRPV4 and TRPC5 — which triggers a cascade (calcium binding calmodulin, activating CaMKII, PKC and the MAPK pathway, ultimately switching on the HAS2 gene) that ends, hours later, in fresh HA being extruded exactly where the load was felt (Kirkness & Scarlata, 2026). The review is based on well-established experimental evidence you can find in the open access paper here.

We describe the whole loop as functioning like a self-lubricating bearing: when mechanical demand goes up, the system automatically manufactures more lubricant, with greater and more sustained mechanical stress producing correspondingly larger, longer-lasting calcium signals and more HA synthesis. Your fascia, in a very real biochemical sense, feels you move and answers by making more of the fluid that lets you keep moving.

Quiet or Riot: two forms of one molecule

Here is where it gets dramatic (in a sense), and where a lot of popular fascia talk goes flat: not all HA does the same job. Long-chain, high-molecular-weight HA (HMW-HA) preferentially binds a receptor called CD44, and that binding promotes tissue stability, hydration, and an anti-inflammatory, homeostatic state — what we call “Quiet” (Kirkness & Scarlata, 2026). 

Short, fragmented, low-molecular-weight HA (LMW-HA), by contrast, preferentially binds a different receptor, RHAMM, and drives cell migration, matrix remodelling and — if it accumulates unchecked — inflammatory signalling, since fragmented HA can also function as a damage-associated molecular pattern, a DAMP, a chemical “something is wrong here” signal.

Healthy fascia oscillates between these two states, quietly maintaining itself most of the time and riotously remodelling when it needs to repair (everyday housekeeping). Chronic stiffness and myofascial pain are associated with the system getting stuck in Riot mode, densifying with fragmented HA that isn’t being cleared as fast as it accumulates (Stecco et al., 2011; Amir et al., 2022).

Where “stuck” actually comes from

So the sensational framing — waterways get stuck — has a real molecular referent. It is not that fascia physically clogs like a drain, but that the balance between HA synthesis, fragmentation, and clearance can fall out of sync, particularly under prolonged immobility layered with low-grade inflammation. When that happens, HA (normally a fluid, shock-absorbing gel) behaves more like a thickened, viscous paste. This is the stuff stiffening tissue planes, impairing microcirculation, and contributing to exactly the kind of restricted, achy symptoms that manual therapists and movement teachers are trying to resolve.

The critical-realist pov

Now the honest part. The CHA axis is a proposed integrative framework, not a settled fact etched in stone. My co-author Suzanne Scarlata and I built it by drawing together strong evidence from fibroblasts and mesenchymal stem cells across many tissue types. 

However, we say explicitly that direct, calcium-dependent evidence in fasciacytes themselves still needs to be demonstrated experimentally, and that the field currently lacks quantitative mechanical thresholds separating helpful loading from harmful loading (Kirkness & Scarlata, 2026). I’m telling you this not to undercut the story but because that’s how science works. So we’re sensational enough to be memorable, precise enough to be honest. 

What’s coming next

Over the next three posts, we’ll get practical. Post two looks at why rotational, twisting movement may be a particularly efficient way to encourage this fluid exchange. Specifically, we advocate for a gentle “wringing” of the tissue, applied within the body’s actual capacity. Post three turns to the opposite end of the intensity spectrum: the case for vigorous exercise as a way of driving out pathologic, DAMP-signalling HA fragments and pathologic cells more thoroughly. And post four brings it together into something you can actually act on today, anchored in the largest systemic study of exercise’s effects on the human body ever conducted.