The Mail Online hails a "breakthrough in treating high blood pressure", saying scientists have discovered how the body regulates it, which could "slash risk of heart attacks and stroke".
But there's a hint of hype around this news as, perhaps surprisingly, the research that prompted this story did not test any new treatments for high blood pressure.
Instead, studies in the laboratory and in mice found genetically engineered mice lacking a protein called ERp44 had low blood pressure. This led the researchers to do other experiments, showing how the protein works with another protein called ERAP1, which is involved in controlling blood pressure.
Overall, this finding has increased researchers' knowledge of how blood pressure is controlled at a molecular level. While it is likely these processes in mice are similar to those of humans, further study would be needed to confirm this.
Even if it is confirmed, as yet the researchers have developed no drugs to target these proteins. Any new treatment aiming to do so would need to be thoroughly tested in the laboratory before it would be safe enough to test on humans.
The study was carried out by researchers from the RIKEN Brain Science Institute and other research centres in Japan.
It was funded by JST International Cooperative Research Project-Solution Oriented Research for Science and Technology, the Japan Society for the Promotion of Science, Scientific Research C, The Moritani Scholarship Foundation, and RIKEN.
The study was published in the peer-reviewed journal Molecular Cell.
The Mail Online headline overstates these findings in two ways – first, this experiment is only in mice and needs to be confirmed in humans. Second, we don't yet know if these findings will lead to treatments for human high blood pressure or other conditions.
This laboratory and animal research studied the function of a protein known as ERp44. Researchers wanted to know more about this protein, which is already known to be involved in helping make sure other cell proteins are made properly and controlling how they are secreted from the cell.
Often, when the function of a protein is not fully understood, researchers start by genetically engineering mice to lack the protein. They then look at what happens to these mice to find out more.
This is what this study has done. This type of study can suggest ways human diseases might be treated, but is at a very early stage and no drugs were involved.
The researchers genetically engineered mice to lack the ERp44 protein. They studied the health and development of these mice, and looked at exactly what knock-on effect a lack of ERp44 had on the cells.
They also identified which proteins ERp44 was normally interacting with and studied the effect of removing this protein in the mice lacking the ERp44 protein.
The researchers found baby mice that lacked the ERp44 protein produced less urine and had changes in the internal structure of their kidneys. Adult mice lacking ERp44 had low blood pressure.
These findings were similar to those known to occur in mice with low levels of the blood pressure-controlling hormone angiotensin. The researchers found angiotensin was being broken down more quickly than normal in ERp44-lacking mice.
The researchers then looked for proteins that interacted with ERp44. They found a protein called ERAP1 and showed how this protein formed a bond with the ERp44 protein. Experiments in cells in the lab suggested ERp44 was stopping ERAP1 from being released from the cells.
This led the researchers to believe that more ERAP1 would be released in ERp44-lacking mice, and this could be responsible for the breakdown of the angiotensin.
To test this, they removed the ERAP1 from blood samples from ERp44-lacking mice using antibodies. As they expected, these ERAP1-depleted samples did not show as much breakdown of angiotensin.
The researchers also found that in mice experiencing severe infection (which usually causes a large drop in blood pressure), the cells produce more ERp44 and ERAP1, and these form more of the ERp44-ERAP1 "complex".
These mice have less of a drop in their blood pressure than mice genetically engineered to have half the normal levels of ERp44. This suggests the extra ERp44-ERAP1 complex helps normal mice stop their blood pressure dropping too low during infection.
The researchers concluded they had showed that, "ERp44 is required for suppressing the release of excess ERAP1 into the bloodstream in order to prevent unfavourable [low blood pressure]."
They reported how variations in the gene encoding ERAP1 have been associated with low blood pressure, psoriasis and a skeletal problem called ankylosing spondylitis, and that, "development of specific drugs targeting ERAP1 activity may contribute to treatment of these diseases".
This animal research has identified a role for certain proteins in controlling blood pressure. Studies like this give clues as to how human biology works and how it can be fixed when it goes wrong.
While the researchers suggest drugs targeting the proteins identified could help develop drugs to treat abnormal blood pressure, these drugs have not yet been developed.
Researchers will need to develop such chemicals and thoroughly test their effects in animals first before they can be tested in humans.
As such, this is early stage research, and there has not been a "treatment breakthrough" yet, because no treatment exists.