High blood pressure can accelerate osteoarthritis joint damage via a newly identified hormone pathway

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by Sanjukta Mondal, Medical Xpress

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Hypertension accelerates OA through AVP-AVPR1A signaling. Credit: Science (2026). DOI: 10.1126/science.aed8207

For millions of people, osteoarthritis slowly breaks down the joints, bringing pain, swelling and stiffness that make free movement harder with time. It is largely a condition of age, with 73% of those living with it older than 55. For years, the wear and tear that comes with aging and physical trauma was considered a major driver of the disease. A recent study published in Science, however, points to a metabolic disease that is also highly common among this demographic as a contributing factor in osteoarthritis progression.

A look at national health data from 36,820 Korean adults ages 45 and older revealed that high blood pressure was linked to osteoarthritis, with stronger associations in more severely damaged knees.

In mouse models, the researchers saw that hypertension actively drives joint breakdown in aging or injured joints. The damaging mechanism was coordinated by a brain hormone and a hormone receptor found in joints. These two components created conditions that ramped up destructive enzymes that break down cartilage. At the same time, they suppressed the production of cartilage components, such as collagen and aggrecan, that joints need to repair themselves.

Burden of bone disease

Osteoarthritis (OA) is a major cause of disability in older adults and affected an estimated 595 million people in 2020. Data from the past 40 years show that the burden of OA is growing, with the total number of cases increasing by 132.2% since 1990.

Despite how common OA is, there is still no treatment that can stop or reverse the disease. Most treatments focus on managing symptoms. To find new treatments that directly target the disease, researchers need a clear understanding of what causes cartilage to break down and what makes the disease worse.

Earlier studies have found links between high blood pressure and osteoarthritis, but the biological connection remained unclear. To explore that connection, the researchers combined analysis of human population data with experiments using mouse disease models.

Using data from the Korea National Health and Nutrition Examination Survey, the team measured whether high blood pressure is independently linked to osteoarthritis. They calculated adjusted odds ratios for both physician-diagnosed disease and X-ray-confirmed knee damage.

To test cause and effect in living organisms, the team performed surgery on male mice to simulate mechanical joint wear and tear. They cut microscopic knee sections and stained them with a dye to measure changes in knee and bone structures.

Experimental schematics for DOCA-salt–induced (C) and genetically hypertensive BPH/2J (D) mouse models. Credit: Science (2026). DOI: 10.1126/science.aed8207

Two stops to damaged cartilage

Gene profiling experiments showed that high blood pressure increases blood levels of a brain hormone called arginine vasopressin (AVP), which travels through the bloodstream and leaks into the joint fluid. Healthy joint cartilage has little to no place for this hormone to bind, but mechanical injury or aging changes that.

Damaged cartilage starts producing a receptor called AVPR1A, which binds the hormone AVP and switches on a gene regulator called NR4A3. This sets off a damaging chain reaction. Cells begin producing excessive amounts of enzymes that break down cartilage while simultaneously reducing the proteins needed to build and maintain it.

The researchers also compared damaged and healthy knee cartilage and joint fluid collected during human total knee replacement surgeries. The damaged human cartilage had higher levels of AVPR1A receptors and a biomarker of the hormone vasopressin, which is responsible for increased blood pressure.

The AVP-AVPR1A axis is required for hypertension-induced acceleration of OA. (P) Proposed model. Credit: Science (2026). DOI: 10.1126/science.aed8207

They also found that removing the AVPR1A gene or injecting a vasopressin receptor antagonist called relcovaptan directly into the knee joint prevented high blood pressure from accelerating cartilage loss. However, treating mice with standard blood pressure medication did not improve the condition of the cartilage.

This study uncovers the biological mechanisms linking hypertension to accelerated osteoarthritis progression. The researchers believe that, now that we know about the AVP-AVPR1A signaling pathway, targeting it could be a smart way to stop hypertension from fast-tracking osteoarthritis and help preserve joints in the people most at risk.

Written for you by our author Sanjukta Mondal, edited by Sadie Harley, and fact-checked and reviewed by Robert Egan—this article is the result of careful human work. We rely on readers like you to keep independent science journalism alive. If this reporting matters to you, please consider a donation (especially monthly). You'll get an ad-free account as a thank-you.

Publication details

Su-Jin Kim et al, Hypertension fuels osteoarthritis through neuroendocrine signaling, Science (2026). DOI: 10.1126/science.aed8207

Chunyi Wen et al, Osteoarthritis as a vascular disease, Science (2026). DOI: 10.1126/science.ael3784

Journal information: Science

Key medical concepts

High Blood PressureOsteoarthritisArginine Vasopressin

Clinical categories

OrthopedicsCardiologyHealthy agingCommon illnesses & Prevention Who's behind this story?

Sanjukta Mondal

Master's in Chemistry. Freelance science journalist and communicator. Published in Chemistry World, BioSpace, and The Hindu. Full profile →

Sadie Harley

BSc Life Sciences & Ecology. Microbiology lab background with pharmaceutical news experience in oil, gas, and renewable industries. Full profile →

Robert Egan

Bachelor's in mathematical biology, Master's in creative writing. Well-traveled with unique perspectives on science and language. Full profile →

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