A protein discovered in the brain may hold the key to understanding why your skin condition could be affecting your heart.
For years, doctors have observed a troubling connection: people with psoriasis, particularly severe cases, are more likely to develop cardiovascular disease. The chronic inflammation that causes red, scaly skin patches was thought to also silently damage blood vessels. Now, scientists are investigating a specific protein called sortilin as a potential missing piece in this puzzle, potentially serving as a measurable indicator of hidden—or subclinical—atherosclerosis in psoriasis patients.
Psoriasis is far more than a skin condition; it's a systemic inflammatory disease. Imagine your immune system is constantly sounding a false alarm, not just in your skin but throughout your entire body.
This persistent state of inflammation contributes to the initiation and progression of atherosclerosis—the buildup of fatty plaques in your arteries2 .
In atherosclerosis, the inner lining of the arteries becomes damaged, and inflammatory cells, lipids, and other substances accumulate, forming plaques that can narrow blood vessels or rupture, leading to heart attacks or strokes6 .
Immune system activation leads to chronic skin inflammation
Inflammatory markers circulate throughout the body
Blood vessel walls become inflamed and damaged
Plaques form in arteries, narrowing blood flow
Increased risk of heart attack, stroke, and other complications
Sortilin, encoded by the SORT1 gene, is a multifaceted receptor protein initially identified in the brain1 8 . Think of it as a cellular traffic director.
It primarily resides inside cells (about 90% of it), where it helps shuttle other proteins to their correct destinations, such as the cell surface or to lysosomes for degradation8 .
Sortilin's role in heart disease is complex and multifaceted. It influences atherosclerosis through several key mechanisms:
Interactive chart showing sortilin's role in atherosclerosis pathways
(In a real implementation, this would be a dynamic chart)
A 2024 study published in the Journal of Clinical Practice and Research directly investigated the potential of sortilin as a marker for subclinical atherosclerosis in psoriasis patients9 .
Researchers designed a case-control study to gather objective data. The following table outlines the groups and key measurements taken.
| Aspect | Psoriasis Patient Group (n=33) | Healthy Control Group (n=33) |
|---|---|---|
| Purpose | To assess sortilin levels and arterial health | To provide a baseline for comparison |
| Measurements |
|
|
The study yielded several critical results, with one standing out as particularly significant.
| Measurement | Finding in Psoriasis Group vs. Controls | Statistical Significance |
|---|---|---|
| Serum Sortilin Level | No significant difference (6.20 vs 7.82 ng/mL) | p=0.729 |
| Right CIMT | Significantly higher | p=0.012 |
| Left CIMT | Significantly higher | p=0.020 |
| FIMT | No significant difference | Not significant |
| Sortilin vs. PASI | No correlation with disease severity | p=0.597 |
Despite the lack of a difference in circulating sortilin levels, the crucial discovery was a positive correlation between serum sortilin levels and right CIMT in the psoriasis patient group9 . This means that within the group of psoriasis patients, those with higher sortilin levels tended to have thicker carotid artery walls—a direct sign of subclinical atherosclerosis.
| Research Tool | Function in the Experiment |
|---|---|
| ELISA Kits | To measure the concentration of soluble sortilin in blood serum samples. |
| High-Resolution Ultrasonography | To non-invasively and accurately measure the intima-media thickness of carotid and femoral arteries. |
| siRNA (Small Interfering RNA) | A molecular tool used in lab studies to "silence" the SORT1 gene, allowing researchers to observe what happens when sortilin is absent7 . |
| Apoe−/− and Ldlr−/− Mice | Genetically modified mouse models that develop atherosclerosis, used to study the disease's mechanisms and test potential treatments1 4 . |
The 2024 study suggests that while a single measurement of blood sortilin might not distinguish a psoriasis patient from a healthy individual, it could still be valuable within the psoriasis population for identifying those with accelerated arterial aging9 .
This aligns with the known biology of sortilin. Most of it is intracellular, so blood levels may not fully reflect its activity in specific tissues like the artery wall or liver8 . The correlation with CIMT supports the theory that sortilin is actively involved in the disease process linking psoriasis and cardiovascular disease.
However, the scientific community has encountered complexities. Some studies have failed to find a strong association between plasma sortilin and coronary artery disease in other patient groups5 , highlighting the need for more research to standardize measurements and identify which specific sortilin-related pathways are most critical.
The investigation into sortilin is moving in several exciting directions:
The journey to understand the hidden links between psoriasis and heart disease is ongoing. Sortilin has emerged as a compelling character in this story—a multifunctional protein that sits at the crossroads of inflammation, cholesterol metabolism, and vascular health. While not yet a standard clinical test, the evidence suggests that sortilin is more than a bystander. It appears to be an active participant in the accelerated atherosclerosis that can accompany psoriasis, offering scientists a promising new target for future breakthroughs that could protect both the skin and the heart.
This article is based on a synthesis of current scientific literature and is intended for informational purposes only. It is not medical advice. Please consult with a healthcare professional for any health concerns or treatment decisions.