Research press release


Nature Medicine

A role for adenosine in sickle-cell anemia



Y Xiaたちは、鎌状赤血球症のマウスとヒトでは血液中のアデノシン濃度が上昇して、赤血球の鎌状化と破壊を促進することを発見した。この作用は特殊なアデノシン受容体の活性化に依存しており、その結果、ヘモグロビンの酸素親和性を低下させる2,3-ジホスホグリセリン酸という赤血球特異的代謝産物がつくられる。このアデノシン受容体を標的とする薬剤ができれば、鎌状赤血球貧血患者に有効かもしれない。

Excessive adenosine signalling has a pathological role in sickle-cell anaemia, pointing to new therapeutic possibilities against this disease, reports a new study published online this week in Nature Medicine.

In sickle-cell anaemia, red blood cells — erythrocytes — acquire an abnormal shape. Lack of oxygen can be the initial trigger to induce this “sickling”, which eventually leads to organ damage in patients.

Yang Xia and her team found that the concentration of adenosine in the blood was elevated in mice and humans with sickle-cell disease, promoting erythrocyte sickling and rupture. These effects depended on the activation of a specific adenosine receptor, which results in the production of 2,3-diphosphoglycerate, an erythrocyte-specific metabolite that decreases the oxygen binding affinity of hemoglobin. Drugs that target this adenosine receptor may have beneficial effects in people with sickle-cell anaemia.

doi: 10.1038/nm.2280


メールマガジンリストの「Nature 関連誌今週のハイライト」にチェックをいれていただきますと、毎週各ジャーナルからの最新の「注目のハイライト」をまとめて皆様にお届けいたします。