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Decode the Environment Variation of Targeted Aldosterone Inducer and siLencer (DETAIL)

2026年9月30日 更新者:Nathaphong Dejthida、DejthidaNathaphong

Clinical outcome to identify and analyze the epigenetic, phenotypic, protein variation, metabolites of CYP450 Family 11 Subfamily B, both 1 and 2, human-associated aldosterone protein release, and signaling inhibitory pathways post-aldosterone-mineralocorticoid interaction.

We will include clinical studies (RCTs, cohort, case-control/series/report) from fresh human specimens. We will exclude animal studies, studies generated from cell culture, and aldosterone synthesis.

To systematically review and synthesize the literature on the main 2 questions Question 1: Which environment induces CYP11B1 or CYP11B2 activation causing hyperaldosteronemia in hypertension patients? Question 2: Which intracellular signal silences aldosterone-MR activity? For Individual Participant Data Meta-analysis, data will be extracted from final analysis articles from the framework of the data selection process only; the effect measurement and multi-variable model meta-analysis will be performed.

Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.

Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone

Secondary Objective 2:

Sub-group analysis effect measurement following;

  • Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia
  • Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action
  • Analyze possible mechanisms of signal that are silent aldosterone-MR activity
  • Differentiation of free aldosterone and attached aldosterone

Secondary Objective 2:

● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone

研究概览

详细说明

Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.

Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone

Secondary Objective 2:

Sub-group analysis effect measurement following;

  • Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia
  • Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action
  • Analyze possible mechanisms of signal that are silent aldosterone-MR activity
  • Differentiation of free aldosterone and attached aldosterone

Secondary Objective 2:

● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone Axin-CK1-GSK3-APC-Beta-catenin complex

研究类型

介入性

注册 (估计的)

100

阶段

  • 不适用

联系人和位置

本节提供了进行研究的人员的详细联系信息,以及有关进行该研究的地点的信息。

学习联系方式

  • 姓名:Nathaphong Dejthida, Medical Degree
  • 电话号码:+66819220662
  • 邮箱:bnnatto@gmail.com

学习地点

    • Bangkok
      • Vadhana、Bangkok、泰国、10110
        • Investigation Center
        • 接触:
          • Nathaphong Dejthida, Medical Degree
          • 电话号码:+66819220662
          • 邮箱:bnnatto@gmail.com
        • 接触:
        • 首席研究员:
          • Nathaphong Dejthida, Medical Degree

参与标准

研究人员寻找符合特定描述的人,称为资格标准。这些标准的一些例子是一个人的一般健康状况或先前的治疗。

资格标准

适合学习的年龄

18年 至 100年 (成人、年长者)

接受健康志愿者

不

有资格学习的性别

全部

描述

Inclusion Criteria:

  • Human birth in all sex chromosomes; evidence of systemic arterial hypertension, both treated and untreated.
  • Evidence of living with owned systemic/arterial hypertension by one of the following;
  • Quantitative: Blood pressure number higher than the normal range by each protocol in mmHg unit in any arm of study.
  • Qualitative: Clarify whether both retrospective, observational, or intervention study of blood pressure, and clearly clarify the number of hypertension participants in the article.

Exclusion Criteria:

  • Under 18 years old
  • Specimens of studies not from humans or human specimens but not from an actual living hypertension patient, such as cell culture, in vitro synthesis from laboratory synthesis
  • No evidence of hypertension in the main study
  • Study of imaging confirms adrenal tumor in all types of histopathology results.

学习计划

本节提供研究计划的详细信息,包括研究的设计方式和研究的衡量标准。

研究是如何设计的?

设计细节

  • 主要用途:放映
  • 分配:非随机化
  • 介入模型:并行分配
  • 屏蔽:无(打开标签)

武器和干预

参与者组/臂
干预/治疗
实验性的:Hypertensive Hyperaldosteronemia

Evidence of synthesis of aldosterone and/or degradation of inactive forms of aldosterone, which focuses on

  • CYP450 Family 11 Subfamily B
  • Aldosterone protein
  • Beta-catenin
  • Axin-CK1-GSK3-APC complex

Medical treatment that interferes with free aldosterone levels and reports systolic blood pressure deviation

The non-medical intervention includes MIS, Open surgery, and intravascular guide treatment aim to treat hypetension and lower aldosterone level.

有源比较器:Hypertensive normoaldosteronemia

Evidence of synthesis of aldosterone and/or degradation of inactive forms of aldosterone, which focuses on

  • CYP450 Family 11 Subfamily B
  • Aldosterone protein
  • Beta-catenin
  • Axin-CK1-GSK3-APC complex

Medical treatment that interferes with free aldosterone levels and reports systolic blood pressure deviation

The non-medical intervention includes MIS, Open surgery, and intravascular guide treatment aim to treat hypetension and lower aldosterone level.

研究衡量的是什么?

主要结果指标

结果测量
措施说明
大体时间
Aldosterone circulation profile
大体时间:12 months

The result, both qualitative and quantitative, from aldosterone synthesis to degradation and elimination via urine.

12 months
Aldoseterone synthesis profile
大体时间:12 months

Focus on both quantitative and qualitative evidence of aldosterone, CYP11B1, andand CYP11B2 protein

12 months

次要结果测量

结果测量
措施说明
大体时间
Degradation Profile
大体时间:12 months

Focus on the ratio of degradation activity of the inactive form of aldosterone and the inhibitory competitor inhibits the cell product from the aldosterone-mineralocorticoid receptor. Axin-CK1-GSK3-APC complex profile is indicated

12 months

合作者和调查者

在这里您可以找到参与这项研究的人员和组织。

研究记录日期

这些日期跟踪向 ClinicalTrials.gov 提交研究记录和摘要结果的进度。研究记录和报告的结果由国家医学图书馆 (NLM) 审查,以确保它们在发布到公共网站之前符合特定的质量控制标准。

研究主要日期

学习开始 (估计的)

2026年10月10日

初级完成 (估计的)

2027年2月10日

研究完成 (估计的)

2028年2月5日

研究注册日期

首次提交

2026年7月28日

首先提交符合 QC 标准的

2026年7月31日

首次发布 (实际的)

2026年8月6日

研究记录更新

最后更新发布 (实际的)

2026年10月1日

上次提交的符合 QC 标准的更新

2026年9月30日

最后验证

2026年9月1日

更多信息

与本研究相关的术语

计划个人参与者数据 (IPD)

计划共享个人参与者数据 (IPD)?

是的

IPD 计划说明

The recruitment is published data already

药物和器械信息、研究文件

研究美国 FDA 监管的药品

不

研究美国 FDA 监管的设备产品

不

此信息直接从 clinicaltrials.gov 网站检索,没有任何更改。如果您有任何更改、删除或更新研究详细信息的请求,请联系 register@clinicaltrials.gov. clinicaltrials.gov 上实施更改,我们的网站上也会自动更新.

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