Renal Inflammation: Mechanisms and Consequences

肾脏炎症：机制和后果

• 批准号: 7230971
• 负责人: WILLIAM Evans MITCH
• 金额: $ 98.58万
• 依托单位: BAYLOR COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-05-01 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7230971
• 关键词: Renal; Inflammation; Mechanisms; Consequences

DESCRIPTION (provided by applicant) The O'Brien Center for Renal Inflammation has the mission of furthering our understanding of the mechanisms involved in the initiation, maintenance, and resolution of inflammation in renal disease. Renal inflammation is recognized to have a critical role in the pathogenesis of acute renal failure, glomerulonephritis, diabetic nephropathy, hypertension, and progressive renal disease. In this Center application, we have brought together scientists with expertise in different aspects of inflammation to provide a cohesive and comprehensive investigation of the mechanisms involved in renal inflammation. The multidisciplinary approach will focus on both proinflammatory and anti-inflammatory mechanisms with an emphasis on molecules that have either not received much attention (e.g., uric acid) or that have only recently been identified as having a role in inflammation. The latter includes new chemokines (CXCL16), new adhesion molecules (JAM family), the recently discovered Slit/Robo family, the signaling molecule Smad7, and stanniocalcin. A pathology core that focuses on the role of these molecules in human disease will provide clinical relevance and will be a mechanism for translating basic science observations for potential future clinical research application. The Center will also train fellowship candidates for a career in academic nephrology (in concert with a T-32 training grant which is currently under review), help initiate the careers of junior investigators (via the DR/P&F program), and provide a strong interaction with the other Centers at Baylor that also focus on the inflammatory response (such as the Biology of Inflammation Center). The integrated, multidisciplinary, synergistic and comprehensive approach to study renal inflammation should provide a better understanding of the pathogenesis of renal disease and may provide new therapeutic insights.

描述（由申请人提供）

项目成果

Atrogin-1 affects muscle protein synthesis and degradation when energy metabolism is impaired by the antidiabetes drug berberine.

• DOI: 10.2337/db10-0207
• 发表时间: 2010-08
• 期刊: Diabetes
• 影响因子: 7.7
• 作者: Wang H;Liu D;Cao P;Lecker S;Hu Z
• 通讯作者: Hu Z

AT1A-mediated activation of kidney JNK1 and SMAD2 in obstructive uropathy: preservation of kidney tissue mass using candesartan.

• DOI: 10.1152/ajprenal.00452.2003
• 发表时间: 2004-09
• 期刊: American journal of physiology. Renal physiology
• 作者: Ann Wamsley-Davis;R. Padda;L. Truong;C. C. Tsao-C.;Ping Zhang;D. Sheikh-Hamad

Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice.

• DOI: 10.1172/jci38770
• 发表时间: 2009-10-01
• 期刊: The Journal of clinical investigation
• 作者: Hu, Zhaoyong;Wang, Huiling;Mitch, William E
• 通讯作者: Mitch, William E

Overexpression of stanniocalcin-1 inhibits reactive oxygen species and renal ischemia/reperfusion injury in mice.

• DOI: 10.1038/ki.2012.223
• 发表时间: 2012-10
• 期刊: Kidney international
• 影响因子: 19.6

PTEN inhibition improves muscle regeneration in mice fed a high-fat diet.

• DOI: 10.2337/db09-1155
• 发表时间: 2010-06
• 期刊: Diabetes
• 影响因子: 7.7
• 作者: Hu Z;Wang H;Lee IH;Modi S;Wang X;Du J;Mitch WE
• 通讯作者: Mitch WE