The role of innate immune system in potassium deficiency

2023 Fiscal Year Final Research Report

• Project/Area Number: 22K16225
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53040:Nephrology-related
• Research Institution: Jichi Medical University
• Principal Investigator: Komada Takanori 自治医科大学, 医学部, 講師 (90824730)
• Project Period (FY): 2022-04-01 – 2024-03-31
• Keywords: 慢性腎臓病 / 低K血症 / 炎症 / インフラマソーム

Outline of Final Research Achievements

Hypokalaemia is not only the risk of all-cause mortality and cardiovascular death but also the independent risk of chronic kidney disease (CKD) progression. It is known that long-standing hypokalaemia occasionally develops kidney dysfunction, so-called hypokalaemic nephropathy (HN). We investigated the role of inflammasome-composing molecules in the mouse HN model. Inflammatory cells expanded in HN kidneys. This phenotype was highly associated with several inflammasome-related molecules but independent of inflammasome activation. These results indicate the possible interconnection between the pro-inflammatory signalling and the potassium homeostatic pathway.

Free Research Field

腎臓病学

Academic Significance and Societal Importance of the Research Achievements

カリウムは生体に必須の元素であり、K異常症は不整脈などを誘発して生命予後に影響する。K異常による炎症惹起と臓器障害は未だ不明な点が多い。本研究では、低K血症による腎の炎症惹起機序について、その責任細胞と寄与経路を明らかにした。電解質異常における臓器炎症の制御機構の理解につながり、学術的意義がある。本研究の成果は、CKD腎を含めた腎疾患の炎症病態解明と治療法開発につながることが期待できる。