A cell is like an orchestra, where every protein plays its own part. But in progeria, one "tuner" works too hard and drowns out an important note. That note is a chemical mark on the protein that packages DNA. When the mark is there, the cell can repair its genes precisely, like a musician who hears every note. When the mark disappears, the repair goes wrong, and the cell ages faster.
Scientists figured out that the culprit is a protein named HDAC2. It removes this helpful mark. So they tried compounds that interfere with HDAC2. In blood vessel cells from progeria patients, the level of the mark rose, and the cells kept dividing longer and aged less. The combination with lonafarnib, a drug already used to treat this disease, worked especially well.
Now scientists want to develop more precise drugs that act only on HDAC2 and leave other proteins alone. If that works, people with progeria could keep their blood vessels healthy for longer.
Santacruzamate A, which showed the strongest effect in this work, was first isolated from a marine cyanobacterium and named after Santa Cruz Island, where it was found. Despite debate about its selectivity, it remains a useful tool for studying HDAC2 in cells.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.