2014 Angiotensin Gordon Research Conference and Gordon Research Seminar

2014年血管紧张素戈登研究会议暨戈登研究研讨会

• 批准号: 8719379
• 负责人: Lisa A Cassis
• 金额: $ 1万
• 依托单位: GORDON RESEARCH CONFERENCES
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-03-01 至 2015-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8719379
• 关键词: AGTR2 gene; Academia; Acute; Adverse effects; Aging; Agonist; Aldosterone; Aldosterone Receptors; Aldosterone Synthase; Aminopeptidase; Angiopoietin-2; Angiotensin II; Angiotensin II Signaling Pathway; Angiotensin II Type 1 Receptor Blockers; Angiotensin Receptor; Angiotensin-Converting Enzyme Inhibitors; Angiotensinogen; Angiotensins; Ants; Area; Atherosclerosis; Award; Basic Science; Biological Markers; Boxing; Cardiovascular Diseases; Chymase; Clinic; Clinical; Clinical Pathology; Clinical Sciences; Collaborations; Critiques; Data; Development; Diabetes Mellitus; Discipline; Drug resistance; Electrolyte Balance; Enzymes; Epigenetic Process; Event; Fostering; France; Functional disorder; Future; G-Protein-Coupled Receptors; Gender; Generations; Genomics; Head; Heart failure; Hypertension; Hypotension; Industry; Insulin; Insulin Receptor; Intervention; Kentucky; Kidney; Leadership; Metabolic; Mineralocorticoid Receptor; Modality; Names; Nerve Degeneration; Netherlands; Obesity; Oral; Oranges; Paris, France; Pathway interactions; Patients; Peptides; Peptidyl-Dipeptidase A; Pharmaceutical Preparations; Pharmacologic Substance; Play; Postdoctoral Fellow; Pre-Eclampsia; Process; Proteomics; Published Comment; Receptor Signaling; Receptor, Angiotensin, Type 1; Renin; Renin-Angiotensin System; Renin-Angiotensin-Aldosterone System; Research; Research Personnel; Resistant Hypertension; Role; Running; Scientific Advances and Accomplishments; Scientist; Series; Signal Pathway; Signal Transduction; Signs and Symptoms; Speed; Stress; Students; Syndrome; System; Techniques; Testing; Texas; Time; Tissues; Travel; Universities; Voting; aminopeptidase B; analog; angiotensin I (1-7); angiotensin II, des-Asp(1)-des-Arg(2)-Ile(5)-; bench to bedside; blood pressure regulation; career; clinically relevant; college; extracellular; glutamyl aminopeptidase; graduate student; hyperkalemia; inhibitor/antagonist; meetings; member; posters; public health relevance; receptor; respiratory; social; symposium; tool; urinary

DESCRIPTION (provided by applicant): The renin-angiotensin system (RAS) plays a vital role in virtually every cardiovascular disease, and drugs blocking this system are currently widely used. Three classes can be distinguished (renin inhibitors, ACE inhibitors and angiotensin II type 1 (AT1) receptor antagonists), which in essence all block the same renin- angiotensin-AT1 receptor pathway. Although for many years it was argued 'the more blockade, the better', recent trials (ONTARGET, ALTITUDE) have shown that this is not the case. In fact, at perhaps slightly more benefit, there are also more side effects (hypotension, hyperkalemia, renal dysfunction). Clearly therefore, we have reached the maximum benefit that can be obtained from blocking this pathway, and we need new pathways to interfere with. Indeed, in the last few years multiple new RAS pathways have emerged that are worth exploring: the (pro) renin receptor, the AT2 receptor (which appears to be stimulated by an angiotensin II metabolite, angiotensin-(2-8)) and the ACE2-angiotensin-(1-7)-Mas receptor pathway. In addition, angiotensin II stimulates the synthesis and release of aldosterone (hence the system is also called the renin-angiotensin- aldosterone system, RAAS). Aldosterone receptor antagonists are now important tools in resistant hypertension, whereas simultaneously new aldosterone receptors emerge (e.g., GPR30), and aldosterone synthase inhibitors are being tested as potential treatment modalities. The first AT2 receptor (ant) agonists are currently being evaluated clinically, and this is also tre for various drugs interfering with the ACE2- angiotensin-(1-7)-Mas receptor pathway (e.g., in acute respiratory stress syndrome). Clearly, at present, the RA(A)S field is rapidly moving ''beyond'' angiotensin II, the classical end-product of this system, and many new drugs start to emerge, also including drugs that acts on one specific signaling pathway of angiotensin II (''biased AT1 receptor agonists''). The Angiotensin GRC is the only meeting where these topics come together in one meeting. It is THE discussion place for the latest discoveries in the RAS, involving basic scientists and clinicians, and combined with a GRS Seminar also attracts a lot of young investigators from academia and industry. Allowing their interaction will help to move the field forward, thus making multiple new drugs available to patients ASAP.

描述（由申请人提供）：肾素-血管紧张素系统（RAS）在几乎所有心血管疾病中都起着至关重要的作用，并且阻断该系统的药物目前被广泛使用。可分为三类（肾素抑制剂、ACE 抑制剂和血管紧张素 II 1 型 (AT1) 受体拮抗剂），它们本质上都阻断相同的肾素-血管紧张素-AT1 受体途径。尽管多年来人们一直认为“封锁越多越好”，但最近的试验（ONTARGET、ALTITUDE）表明情况并非如此。事实上，虽然好处可能稍微多一些，但副作用也更多（低血压、高钾血症、肾功能障碍）。因此，显然，我们已经达到了通过阻断这条途径可以获得的最大利益，并且我们需要新的途径来干扰。事实上，在过去几年中，出现了多种值得探索的新 RAS 通路：（原）肾素受体、AT2 受体（似乎受到血管紧张素 II 代谢物血管紧张素-(2-8) 的刺激）和ACE2-血管紧张素-(1-7)-Mas 受体途径。此外，血管紧张素II刺激醛固酮的合成和释放（因此该系统也称为肾素-血管紧张素-醛固酮系统，RAAS）。醛固酮受体拮抗剂现在是治疗顽固性高血压的重要工具，同时新的醛固酮受体出现（例如GPR30），并且醛固酮合酶抑制剂正在作为潜在的治疗方式进行测试。第一个 AT2 受体 (ant) 激动剂目前正在临床上进行评估，这也是针对干扰 ACE2-血管紧张素-(1-7)-Mas 受体途径的各种药物（例如，在急性呼吸应激综合征中）的评估。显然，目前 RA(A)S 领域正在迅速“超越”血管紧张素 II（该系统的经典最终产品），并且许多新药物开始出现，其中还包括作用于一种特定信号通路的药物血管紧张素 II（“偏向 AT1 受体激动剂”）。血管紧张素 GRC 是唯一将这些主题集中在一次会议上的会议。它是RAS最新发现的讨论场所，涉及基础科学家和临床医生，与GRS研讨会相结合也吸引了很多来自学术界和工业界的年轻研究人员。允许它们相互作用将有助于推动该领域的发展，从而尽快为患者提供多种新药。