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NCT Number: NCT07129330

RSPO3/SDC-1 Pathway Dysfunction in Alveolar Repair After ARDS in Older Adults

Acute respiratory distress syndrome (ARDS) is a serious lung condition in which fluid builds up in the air sacs, making it hard to breathe and often requiring intensive care. Older adults fare worse because their lung-lining cells lose the ability to heal properly after injury This study will explore two key molecules-RSPO3 and Syndecan-1 (SDC-1)-that normally help alveolar (air-sac) cells regenerate. We will collect small blood samples from ARDS patients and, when patients undergo elective lung surgery, tiny pieces of healthy lung tissue. In the lab, we will also grow three-dimensional "lung organoids" from these samples to see how boosting or blocking RSPO3/SDC-1 affects cell repair

Our goals are to:

Measure RSPO3/SDC-1 activity alongside inflammatory markers (e.g., IL-6, TNF-α) to understand their roles in age-related repair failure.

Build an integrated platform for early diagnosis, disease monitoring, and treatment evaluation in older ARDS patients.

Identify molecular targets that could lead to new therapies, helping older adults recover lung function more effectively.

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Key information

Conditions

Acute Respiratory Distress Syndrome (ARDS) Age-related Impaired Alveolar Epithelial Repair Lung Diseases Respiration Disorders Respiratory Distress Syndrome Respiratory Tract Diseases

Sex eligibility

All sexes

Study type

Observational

Primary location

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

Clinical diagnosis of acute respiratory distress syndrome (ARDS) according to the Berlin Definition Age ≥ 65 years at enrollment First diagnosis of ARDS made within 24 hours prior to study entry Receiving either spontaneous (non-invasive) breathing support or invasive mechanical ventilation

Exclusion criteria

Coexisting severe cardiac, hepatic or renal failure (NYHA Class III-IV) Active pulmonary infection (e.g. pneumonia or lung abscess) Significant coagulation disorders Receipt of any cytokine-based therapy within the past 3 months Participation in another interventional clinical study within the past 3 months

Treatment and study plan

RSPO3/SDC-1 pathway profiling assay

Procedure

Peripheral Blood: 5 mL collected into EDTA tubes; PBMCs isolated within 2 h for RT-qPCR analysis of RSPO3/SDC-1 mRNA and sandwich ELISA quantification of protein levels.

Saliva: 2-3 mL unstimulated saliva naturally expectorated into sterile tubes, kept at 4 °C and processed within 2 h (centrifuged, aliquoted) before -80 °C storage Subcutaneous Fat: 100-200 mg obtained during elective procedures, preserved in RNAlater at 4 °C for 24 h, then frozen at -80 °C 3D Alveolar Organoid Assay: Lung tissue-derived organoids are cultured in Matrigel and treated ex vivo with recombinant RSPO3 or SDC-1 neutralizing antibody; epithelial repair is assessed over 7 days by Ki-67 immunostaining and wound-closure measurement

Blood and Saliva

Procedure

Peripheral Blood: 5 mL collected into EDTA tubes; PBMCs isolated within 2 h for RT-qPCR analysis of RSPO3/SDC-1 mRNA and sandwich ELISA quantification of protein levels.

Saliva: 2-3 mL unstimulated saliva naturally expectorated into sterile tubes, kept at 4 °C and processed within 2 h (centrifuged, aliquoted) before -80 °C storage

Primary outcomes

  1. Correlation Between Peripheral Blood RSPO3/SDC-1 Pathway Activity and Alveolar Epithelial Injury Marker Levels

    Time frame: Baseline (within 24 hours of ARDS diagnosis)

    Quantify RSPO3 and Syndecan-1 expression in peripheral blood (by RT-qPCR and ELISA) and measure alveolar injury biomarkers (SP-A, SP-D) in serum. Calculate Pearson or Spearman correlation coefficients between RSPO3/SDC-1 levels and SP-A/SP-D concentrations in elderly ARDS patients at baseline.

Secondary outcomes

  1. Effect of RSPO3/SDC-1 Pathway Modulation on Alveolar Organoid Repair Capacity

    Time frame: Within 14 days of organoid establishment

    Assess lung organoid epithelial repair by measuring (1) percentage of Ki-67-positive cells and (2) wound-closure area in 3D alveolar organoid cultures treated with recombinant RSPO3 protein or SDC-1 neutralizing antibody versus untreated controls.

Other outcomes

  1. Diagnostic Performance of the RSPO3/SDC-1-Based Integrated Platform

    Time frame: Upon completion of all sample processing (estimated by study end)

    Evaluate the multi-marker platform combining RSPO3/SDC-1 activity and inflammatory cytokines (IL-6, TNF-α) by calculating AUC, sensitivity, specificity, PPV, and NPV for predicting impaired alveolar repair in elderly ARDS patients.

Study contacts

Contact information is provided by the study sponsor or research team.

Jiang

CONTACT

[email protected]

+86 13817719616

Sponsors and collaborators

Lead sponsor

Xinhua Hospital, Shanghai Jiao Tong University School of Medicine

Other

Registry information

Official study title

Role and Mechanisms of RSPO3/SDC-1 Pathway Dysregulation in Impaired Alveolar Epithelial Repair Post-ARDS in Older Adults

Important dates

Study start
2025
Primary completion
2025
Study completion
2029
First posted
Aug 19, 2025
Registry last updated
Aug 19, 2025

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

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This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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