High blood pressure and osteoarthritis, two conditions commonly experienced with age, are not unrelated ailments after all: a Korean research team has shown that the body’s blood-pressure signaling directly accelerates the destruction of joint cartilage. A blood-pressure-regulating hormone secreted in the brain travels through the bloodstream to act remotely on the joints and break down cartilage, a finding expected to offer a clue toward new treatment strategies for osteoarthritis, which has had no cure to date.
 [코리안투데이] A schematic diagram of the mechanism by which the rise in vasopressin caused by high blood pressure promotes cartilage destruction in osteoarthritis © 장형임 기자 |
The Ministry of Science and ICT (Deputy Prime Minister and Minister Bae Kyung-hoon) announced that a joint research team led by Professor Ryu Je-hwang of Chonnam National University and Professor Chun Jang-soo of Inje University has identified the specific molecular mechanism by which high blood pressure worsens osteoarthritis (degenerative arthritis). The study was carried out under the ministry’s basic research programs (including the Leading Research Center and Mid-career Researcher programs) and was published on October 2 in Science, the world’s most authoritative academic journal (local time October 1, 2:00 p.m. EDT). The paper is titled ‘Hypertension fuels osteoarthritis through neuroendocrine signaling.’
Osteoarthritis and high blood pressure frequently appear together in older adults. The two conditions may look like unrelated diseases affecting the joints and blood vessels respectively, but it has long been observed that arthritis tends to be more severe in patients with high blood pressure. Yet the fundamental reason the two worsen in tandem had never been clearly explained, and their relationship long remained an unexplained coincidence.
The team first conducted a detailed analysis of data from the Korea National Health and Nutrition Examination Survey, confirming that people with high blood pressure had a higher prevalence of osteoarthritis and that the more severe the arthritis, the clearer its association with high blood pressure. Next, through experiments using two types of mouse models in which high blood pressure had been induced by different methods, the team demonstrated that high blood pressure does indeed accelerate osteoarthritis, and observed that changes extended not only to cartilage damage but also to the subchondral bone beneath it.
At the heart of the mechanism were vasopressin (AVP), a hormone secreted in the brain that regulates blood pressure, and vasopressin receptor 1A (AVPR1A), which receives it. Vasopressin is a neurohormone secreted by the posterior pituitary gland that is involved in regulating the body’s water balance and raising blood pressure. Under high blood pressure, blood vasopressin levels rise, while the vasopressin receptor, which is nearly absent in healthy cartilage, increases sharply when a joint is damaged or aged. As a result, when the elevated vasopressin binds to the increased receptors, signals that break down cartilage are switched on and signals that maintain cartilage are switched off, promoting cartilage destruction.
The team confirmed that when this signaling is activated, the cartilage-degrading enzymes MMP3 and MMP13 increase while type II collagen and aggrecan, which compose and maintain cartilage, decrease. Conversely, when the AVPR1A gene was deleted in mice or when the inhibitor relcovaptan was administered to the joints, cartilage damage caused by high blood pressure was greatly reduced. The team also identified NR4A3 as the key transcription factor that links this signaling to cartilage breakdown, thereby mapping the entire signal-transduction process.
This study is the first to break the long-held notion that arthritis is a disease of the joints alone and to provide actual evidence that a hormone produced in the brain regulates joint health. In particular, by elucidating a context-dependent mechanism of onset in which the signal is not activated indiscriminately but is strongly switched on only when cartilage is already damaged or aged, the work is credited with broadening research that once looked only inside the joint into a whole-body axis linking the brain, hormones and the joint.
For residents and patients, the achievement signals a shift in how osteoarthritis is managed, because it suggests that osteoarthritis must be managed by addressing not only the local joint but also systemic conditions such as blood pressure. In particular, for high-blood-pressure patients who are elderly or who have joint damage, active blood-pressure management may be a way to protect joint health. Furthermore, the findings could serve as a basis for integrated patient-care guidelines that encompass both the assessment of joint health in high-blood-pressure patients and blood-pressure management in osteoarthritis patients, as well as for establishing health and medical policy.
The achievement also carries great significance in that it was completed under the leadership of a purely domestic research team. Professor Chun Jang-soo, a distinguished professor at Inje University who led the study, has now published research as corresponding author in all three of the world’s top science journals: Cell in 2014, Nature in 2019, and now Science. The first authors of the paper were postdoctoral researcher Kim Su-jin (Chonnam National University) and researcher Kim Hyo-eun (Chonnam National University).
Professor Ryu Je-hwang of Chonnam National University said, ‘This achievement suggests that when treating osteoarthritis patients, we must manage not only the local joint but also systemic health conditions such as high blood pressure,’ adding, ‘Going forward, we plan to advance follow-up research toward developing a fundamental arthritis treatment that targets the vasopressin signaling system.’
Kim Sung-soo, director-general for R&D policy at the Ministry of Science and ICT, said, ‘This achievement shows that basic research uncovering the principles behind the onset and progression of disease can be the starting point for developing new treatments,’ and added, ‘We will continue to spare no support so that basic research leads to outcomes that the public can tangibly feel.’
지역 홍보대사 신청 기자양성과정 신청 코리안투데이 지부장 신청 코리안투데이 인천강화코리안브랜드대상 신청 최고경영인대상 신청 소비자만족도대상 신청
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