Acute Respiratory Distress SyndromeNCT04937855
The Mechanism of lncRNA NEAT1 in Alleviating Acute Respiratory Distress Syndrome Through miR-27b Regulated Nrf2 Pathway
An observational study of Acute Respiratory Distress Syndrome and Inflammation, run by Beijing Anzhen Hospital at 1 site in China.
Trial summary
The acute respiratory distress syndrome, formerly known as the acute lung injury (ARDS/ALI), is a critical illness with high mortality due to the lack of effective treatment. The pathogenesis of ARDS/ALI has not been fully elucidated. Read more about this study
- Who is it for?
- Ages 18 to 70 yearsHealthy volunteers can take part
- Conditions the study is for
- Acute Respiratory Distress Syndrome, Inflammation
- How many people
- 425 participants
- Where
- 1 siteChina
- Study dates
- 1 Jul 2021to 31 Dec 2023
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: We included ARDS patients from RICU、EICU、SICU、CCU in Beijing Anzhen hospital between 2020 and 2022
Who may be able to join
- We included patients with acute respiratory distress according to 2012 ARDS Berlin new definition (Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA, 2012, 307(23):2526).
- Acute or progressive dyspnea within 1 week with identify cause;
- Chest radiograph/chest CT showed double lung infiltration, which could not be fully explained by pleural effusion, atelectasis, or nodules;
- Respiratory failure cannot be fully explained by heart failure and fluid overload;
- Hypoxemia, partial pressure of oxygen in arterial blood (PaO2)/oxygen fraction in air (FIO2) <150 mm Hg under PEEP ≥5 cm H2O, (mild ARDS: 200mmHg<PaO2/FiO2≤300mmHg, moderate ARDS: 100mmHg<PaO2/FiO2≤200mmHg, severe ARDS: PaO2/FiO2≤100mmHg);
- 18~70 years old;
- Agree to participate in the trial, and sign the informed consent.
Who cannot join
- Age less than 18 years old;
- Time of hospital stay <24 h;
- Pregnancy;
- Using V-V ECOM;
- Cardiac index <1.5L·ml.min-1.m-2;
- Pulmonary resection;
- Pulmonary embolism ;
- Refused to participate in the study.
Trial locations and contacts
1 site in 1 country.
China1 site
Department of Respiratory and Critical Care Medicine, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases
Beijing, Beijing Municipality, 100029
About this study
The acute respiratory distress syndrome, formerly known as the acute lung injury (ARDS/ALI), is a critical illness with high mortality due to the lack of effective treatment. The pathogenesis of ARDS/ALI has not been fully elucidated. Nuclear factor E2-related factor 2 (Nrf2) plays a key role in regulating lung inflammation and oxidative stress which are closely related to lung injury in ARDS/ALI, but its regulatory mechanism remains unclear. The investigator's provious study shown that microRNA-27b (miR-27b) downregulated Nrf2 to aggravate lung inflammation and histological injury. Furthermore, in lipopolysaccharide (LPS)-induced cell (J774A.1) inflammation model, miR-27b was upregulated while the long non-coding RNA (lncRNA) NEAT1 was downregulated, the putative binding sites of lncRNA NEAT1 and miR-27b were successfully predicted by bioinformatics approach. Thus, the investigators propose that NEAT1 plays as a competing endogenous RNA (ceRNA) to adsorb miR-27b and liberate Nrf2, therefore, to attenuate lung inflammation and related lung injury in ARDS/ALI. This project aims to explore the role of the lncRNA NEAT1/ mir-27b /Nrf2 signal axis in the development and treatment of ARDS/ALI in patients, as well as in LPS-induced ALI animal and cell models by using bioinformatics, molecular biology, histomorphology and clinical phenotype approaches, and to clarify the new mechanism in ARDS/ALI development and to provide new therapeutic targets.
Read the detailed description
Collect blood and BALF from 400 ARDS patients at different time (at check-in, 24, 48 and 72 h after check-in the hospital) and 25 gender and age matching healthy controls. Use RT-PCR to detect the expression of lncRNA NEAT1、miR-27b and Nrf2 in blood and BALF of ARDS patients and health controls. The expressions of inflammatory and oxidative stress associated factors (NLRP3、NF-κB-P65、 p-P65、IκB、p-IκB、HO-1、NQO1、caspase-1、IL-1β、IL-6、IL-18、TNF-α) will be detected by western blot、ELISA and RT-PCR. Moreover, flow cytometry will be adopted to measure the numbers and kinds of cells in BALF. Then, analyze the differences of the expressions of lncRNA NEAT1、miR-27b and Nrf2 in the groups. To explore the correlation of expressions of lncRNA NEAT1、miR-27b and Nrf2 with inflammation and oxidative stress in the groups. Finally, to declare the relative of lncRNA NEAT1、miR-27b and Nrf2 with the time of mechanical ventilation, severity and mortality in 28 days of ARDS patients.
- Conditions
- Acute Respiratory Distress Syndrome, Inflammation
- Being tested
- no intervention
- Keywords
- long non-coding RNA NEAT1, microRNA-27b, nuclear factor E2-related factor 2
- Medical subject headings
- Respiratory Distress Syndrome, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
no interventionOther
no intervention
| Study group | Role | What they receive |
|---|---|---|
| Control group | 25 gender and age matching healthy controls Receives: Other: no intervention | |
| ARDS group 1 | 100 ARDS patients at the time of check in hospital Receives: Other: no intervention | |
| ARDS group 2 | 100 ARDS patients at the time of 24h after check in hospital Receives: Other: no intervention | |
| ARDS group 3 | 100 ARDS patients at the time of 48h after check in hospital Receives: Other: no intervention | |
| ARDS group 4 | 100 ARDS patients at the time of 72h after check in hospital Receives: Other: no intervention |
What is being measured
The primary outcome is the main question the study is designed to answer.
The expression of lncRNA NEAT1 in blood and BALF in all groups
Use RT-PCR to measure the expression of lncRNA NEAT1 in blood and BALF in all groups
Measured: up to 24 day
The expression of miR-27b in blood and BALF in all groups
Use RT-PCR to measure the expression of miR-27b in blood and BALF in all groups
Measured: up to 3 day
The expression of Nrf2 in blood and BALF in all groups
Use RT-PCR and Wsetern blot to measure the expression of Nrf2 in blood and BALF in all groups
Measured: up to 3 day
The expression of inflammatory factors(IL-1β、IL-6、IL-18、TNF-α) in blood and BALF in all groups
Use RT-PCR and ELISA to measure the expression of inflammatory factors(IL-1β、IL-6、IL-18、TNF-α) in blood and BALF in all groups
Measured: up to 3 day
The expression of oxidative stress associated factors in blood and BALF in all groups
Use Western blot to measure the expression of oxidative stress associated factors(NLRP3、NF-κB-P65、 p-P65、IκB、p-IκB、HO-1、NQO1、caspase-1) in blood and BALF in all groups
Measured: up to 3 day
The numbers and kinds of inflammatory cells in BALF and blood in all groups
Use flow cytometry to detect the number of inflammatory cells in BALF and blood in all groups
Measured: up to 3 day
The kinds of inflammatory cells in BALF and blood in all groups
Use flow cytometry to detect the kinds of inflammatory cells(neutrophile、macrophage、 lymphocyte) in BALF and blood in all groups
Measured: up to 3 day
The time of mechanical ventilation of patients in ARDS groups
Record the time of mechanical ventilation of patients in ARDS groups
Measured: up to28 day
The severity of ARDS patients in ARDS groups
Record the severity(PaO2/FiO2、OI、S/F、OSI) of ARDS patients in ARDS groups
Measured: up to 28 day
the mortality in 28 days of ARDS patients
Record the mortality in 28 days of ARDS patients
Measured: up to 28 day
Secondary outcomes (3)
The differences and correlation of the expressions of lncRNA NEAT1、miR-27b and Nrf2 in the groups
Analyse the differences of the expressions of lncRNA NEAT1、miR-27b and Nrf2 in the groups, and to explore the relations between the three(lncRNA NEAT1、miR-27b and Nrf2) in different groups.
Measured: up to 28 day
The correlation of expressions of lncRNA NEAT1、miR-27b and Nrf2 with inflammation and oxidative stress in the groups.
To explore the correlation of expressions of lncRNA NEAT1、miR-27b and Nrf2 with inflammation and oxidative stress in the groups.
Measured: up to 28 day
The relative of lncRNA NEAT1、miR-27b and Nrf2 with the time of mechanical ventilation, severity and mortality in 28 days of ARDS patients
To declare the relative of lncRNA NEAT1、miR-27b and Nrf2 with the time of mechanical ventilation, severity and mortality in 28 days of ARDS patients
Measured: up to 28 day
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 Jun 2021
- Study start1 Jul 2021 (estimated)
- Primary completion31 Dec 2022 (estimated)
- Study completion31 Dec 2023 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Acute Respiratory Distress SyndromeStudies of the same condition, open and under way.
- More trials run by Beijing Anzhen HospitalThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Other
- Time perspective
- Prospective
- Enrolment
- 425 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Beijing Anzhen Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Guangfa Zhu, Beijing Anzhen Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04937855
- Sponsor's protocol ID
- 81970067
- Status last verified
- Jun 2021
- First submitted
- 11 Jan 2020
- Last updated
- 24 Jun 2021
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669.
PubMed 22797452Fan E, Brodie D, Slutsky AS. Acute Respiratory Distress Syndrome: Advances in Diagnosis and Treatment. JAMA. 2018 Feb 20;319(7):698-710. doi: 10.1001/jama.2017.21907.
PubMed 29466596Lu MC, Ji JA, Jiang ZY, You QD. The Keap1-Nrf2-ARE Pathway As a Potential Preventive and Therapeutic Target: An Update. Med Res Rev. 2016 Sep;36(5):924-63. doi: 10.1002/med.21396. Epub 2016 May 18.
PubMed 27192495Wei J, Chen G, Shi X, Zhou H, Liu M, Chen Y, Feng D, Zhang P, Wu L, Lv X. Nrf2 activation protects against intratracheal LPS induced mouse/murine acute respiratory distress syndrome by regulating macrophage polarization. Biochem Biophys Res Commun. 2018 Jun 7;500(3):790-796. doi: 10.1016/j.bbrc.2018.04.161. Epub 2018 Apr 25.
PubMed 29684352Liu Q, Lv H, Wen Z, Ci X, Peng L. Isoliquiritigenin Activates Nuclear Factor Erythroid-2 Related Factor 2 to Suppress the NOD-Like Receptor Protein 3 Inflammasome and Inhibits the NF-kappaB Pathway in Macrophages and in Acute Lung Injury. Front Immunol. 2017 Nov 9;8:1518. doi: 10.3389/fimmu.2017.01518. eCollection 2017.
PubMed 29163554Liu Y, Song M, Zhu G, Xi X, Li K, Wu C, Huang L. Corynoline attenuates LPS-induced acute lung injury in mice by activating Nrf2. Int Immunopharmacol. 2017 Jul;48:96-101. doi: 10.1016/j.intimp.2017.04.029. Epub 2017 May 6.
PubMed 28486213Rajasekaran S, Pattarayan D, Rajaguru P, Sudhakar Gandhi PS, Thimmulappa RK. MicroRNA Regulation of Acute Lung Injury and Acute Respiratory Distress Syndrome. J Cell Physiol. 2016 Oct;231(10):2097-106. doi: 10.1002/jcp.25316. Epub 2016 Feb 4.
PubMed 26790856Wu CT, Huang Y, Pei ZY, Xi X, Zhu GF. MicroRNA-326 aggravates acute lung injury in septic shock by mediating the NF-kappaB signaling pathway. Int J Biochem Cell Biol. 2018 Aug;101:1-11. doi: 10.1016/j.biocel.2018.04.019. Epub 2018 May 1.
PubMed 29727715Ling Y, Li ZZ, Zhang JF, Zheng XW, Lei ZQ, Chen RY, Feng JH. RETRACTED: MicroRNA-494 inhibition alleviates acute lung injury through Nrf2 signaling pathway via NQO1 in sepsis-associated acute respiratory distress syndrome. Life Sci. 2018 Oct 1;210:1-8. doi: 10.1016/j.lfs.2018.08.037. Epub 2018 Aug 17.
PubMed 30121199Ding L, Ni J, Yang F, Huang L, Deng H, Wu Y, Ding X, Tang J. Promising therapeutic role of miR-27b in tumor. Tumour Biol. 2017 Mar;39(3):1010428317691657. doi: 10.1177/1010428317691657.
PubMed 28351320Zhou R, Gong AY, Eischeid AN, Chen XM. miR-27b targets KSRP to coordinate TLR4-mediated epithelial defense against Cryptosporidium parvum infection. PLoS Pathog. 2012;8(5):e1002702. doi: 10.1371/journal.ppat.1002702. Epub 2012 May 17.
PubMed 22615562Signorelli SS, Volsi GL, Pitruzzella A, Fiore V, Mangiafico M, Vanella L, Parenti R, Rizzo M, Volti GL. Circulating miR-130a, miR-27b, and miR-210 in Patients With Peripheral Artery Disease and Their Potential Relationship With Oxidative Stress. Angiology. 2016 Nov;67(10):945-950. doi: 10.1177/0003319716638242. Epub 2016 Jul 11.
PubMed 26980776Li T, Cao H, Zhuang J, Wan J, Guan M, Yu B, Li X, Zhang W. Identification of miR-130a, miR-27b and miR-210 as serum biomarkers for atherosclerosis obliterans. Clin Chim Acta. 2011 Jan 14;412(1-2):66-70. doi: 10.1016/j.cca.2010.09.029. Epub 2010 Sep 29.
PubMed 20888330Huang Y, Huang L, Zhu G, Pei Z, Zhang W. Downregulated microRNA-27b attenuates lipopolysaccharide-induced acute lung injury via activation of NF-E2-related factor 2 and inhibition of nuclear factor kappaB signaling pathway. J Cell Physiol. 2019 May;234(5):6023-6032. doi: 10.1002/jcp.27187. Epub 2018 Dec 24.
PubMed 30584668Song YX, Sun JX, Zhao JH, Yang YC, Shi JX, Wu ZH, Chen XW, Gao P, Miao ZF, Wang ZN. Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA mediated miRNA evasion. Nat Commun. 2017 Aug 18;8(1):289. doi: 10.1038/s41467-017-00304-1.
PubMed 28819095
Study at a glance
From the registry record, last updated by the sponsor on 24 Jun 2021. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Mechanism of lncRNA NEAT1 in Alleviating Acute Respiratory Distress Syndrome Through miR-27b Regulated Nrf2 Pathway
- ClinicalTrials.gov ID
- NCT04937855
- Acronym / sponsor ID
- 81970067
- Conditions
- Acute Respiratory Distress Syndrome, Inflammation
- Keywords
- long non-coding RNA NEAT1, microRNA-27b, nuclear factor E2-related factor 2
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 425 participants (estimated)
- Lead sponsor
- Beijing Anzhen HospitalUniversity, hospital or other
- Study start
- 1 Jul 2021 (estimated)
- Primary completion
- 31 Dec 2022 (estimated)
- Study completion
- 31 Dec 2023 (estimated)
- First posted
- 24 Jun 2021 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The acute respiratory distress syndrome, formerly known as the acute lung injury (ARDS/ALI), is a critical illness with high mortality due to the lack of effective treatment. The pathogenesis of ARDS/ALI has not been fully elucidated. Nuclear factor E2-related factor 2 (Nrf2) plays a key role in regulating lung inflammation and oxidative stress which are closely related to lung injury in ARDS/ALI, but its regulatory mechanism remains unclear. The investigator's provious study shown that microRNA-27b (miR-27b) downregulated Nrf2 to aggravate lung inflammation and histological injury. Furthermore, in lipopolysaccharide (LPS)-induced cell (J774A.1) inflammation model, miR-27b was upregulated while the long non-coding RNA (lncRNA) NEAT1 was downregulated, the putative binding sites of lncRNA NEAT1 and miR-27b were successfully predicted by bioinformatics approach. Thus, the investigators propose that NEAT1 plays as a competing endogenous RNA (ceRNA) to adsorb miR-27b and liberate Nrf2, therefore, to attenuate lung inflammation and related lung injury in ARDS/ALI. This project aims to explore the role of the lncRNA NEAT1/ mir-27b /Nrf2 signal axis in the development and treatment of ARDS/ALI in patients, as well as in LPS-induced ALI animal and cell models by using bioinformatics, molecular biology, histomorphology and clinical phenotype approaches, and to clarify the new mechanism in ARDS/ALI development and to provide new therapeutic targets.
Detailed description
Collect blood and BALF from 400 ARDS patients at different time (at check-in, 24, 48 and 72 h after check-in the hospital) and 25 gender and age matching healthy controls. Use RT-PCR to detect the expression of lncRNA NEAT1、miR-27b and Nrf2 in blood and BALF of ARDS patients and health controls. The expressions of inflammatory and oxidative stress associated factors (NLRP3、NF-κB-P65、 p-P65、IκB、p-IκB、HO-1、NQO1、caspase-1、IL-1β、IL-6、IL-18、TNF-α) will be detected by western blot、ELISA and RT-PCR. Moreover, flow cytometry will be adopted to measure the numbers and kinds of cells in BALF. Then, analyze the differences of the expressions of lncRNA NEAT1、miR-27b and Nrf2 in the groups. To explore the correlation of expressions of lncRNA NEAT1、miR-27b and Nrf2 with inflammation and oxidative stress in the groups. Finally, to declare the relative of lncRNA NEAT1、miR-27b and Nrf2 with the time of mechanical ventilation, severity and mortality in 28 days of ARDS patients.
Study design
- Observational model
- Other
- Time perspective
- Prospective
- Number of arms
- 5
| Arm | Type | Receives |
|---|---|---|
| Control group | – | Other: no intervention25 gender and age matching healthy controls |
| ARDS group 1 | – | Other: no intervention100 ARDS patients at the time of check in hospital |
| ARDS group 2 | – | Other: no intervention100 ARDS patients at the time of 24h after check in hospital |
| ARDS group 3 | – | Other: no intervention100 ARDS patients at the time of 48h after check in hospital |
| ARDS group 4 | – | Other: no intervention100 ARDS patients at the time of 72h after check in hospital |
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- We included ARDS patients from RICU、EICU、SICU、CCU in Beijing Anzhen hospital between 2020 and 2022
Key inclusion criteria (7 listed)
- We included patients with acute respiratory distress according to 2012 ARDS Berlin new definition (Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA, 2012, 307(23):2526).
- Acute or progressive dyspnea within 1 week with identify cause;
- Chest radiograph/chest CT showed double lung infiltration, which could not be fully explained by pleural effusion, atelectasis, or nodules;
- Respiratory failure cannot be fully explained by heart failure and fluid overload;
- Hypoxemia, partial pressure of oxygen in arterial blood (PaO2)/oxygen fraction in air (FIO2) <150 mm Hg under PEEP ≥5 cm H2O, (mild ARDS: 200mmHg<PaO2/FiO2≤300mmHg, moderate ARDS: 100mmHg<PaO2/FiO2≤200mmHg, severe ARDS: PaO2/FiO2≤100mmHg);
Key exclusion criteria (8 listed)
- Age less than 18 years old;
- Time of hospital stay <24 h;
- Pregnancy;
- Using V-V ECOM;
- Cardiac index <1.5L·ml.min-1.m-2;
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| no interventionno intervention | Other | ARDS group 1, ARDS group 2, ARDS group 3, ARDS group 4, Control group |
Primary outcome
The expression of lncRNA NEAT1 in blood and BALF in all groups
Time frame: up to 24 day
Use RT-PCR to measure the expression of lncRNA NEAT1 in blood and BALF in all groups
The expression of miR-27b in blood and BALF in all groups
Time frame: up to 3 day
Use RT-PCR to measure the expression of miR-27b in blood and BALF in all groups
The expression of Nrf2 in blood and BALF in all groups
Time frame: up to 3 day
Use RT-PCR and Wsetern blot to measure the expression of Nrf2 in blood and BALF in all groups
The expression of inflammatory factors(IL-1β、IL-6、IL-18、TNF-α) in blood and BALF in all groups
Time frame: up to 3 day
Use RT-PCR and ELISA to measure the expression of inflammatory factors(IL-1β、IL-6、IL-18、TNF-α) in blood and BALF in all groups
The expression of oxidative stress associated factors in blood and BALF in all groups
Time frame: up to 3 day
Use Western blot to measure the expression of oxidative stress associated factors(NLRP3、NF-κB-P65、 p-P65、IκB、p-IκB、HO-1、NQO1、caspase-1) in blood and BALF in all groups
The numbers and kinds of inflammatory cells in BALF and blood in all groups
Time frame: up to 3 day
Use flow cytometry to detect the number of inflammatory cells in BALF and blood in all groups
The kinds of inflammatory cells in BALF and blood in all groups
Time frame: up to 3 day
Use flow cytometry to detect the kinds of inflammatory cells(neutrophile、macrophage、 lymphocyte) in BALF and blood in all groups
The time of mechanical ventilation of patients in ARDS groups
Time frame: up to28 day
Record the time of mechanical ventilation of patients in ARDS groups
The severity of ARDS patients in ARDS groups
Time frame: up to 28 day
Record the severity(PaO2/FiO2、OI、S/F、OSI) of ARDS patients in ARDS groups
the mortality in 28 days of ARDS patients
Time frame: up to 28 day
Record the mortality in 28 days of ARDS patients
3 secondary outcomes
The differences and correlation of the expressions of lncRNA NEAT1、miR-27b and Nrf2 in the groups
Time frame: up to 28 day
The correlation of expressions of lncRNA NEAT1、miR-27b and Nrf2 with inflammation and oxidative stress in the groups.
Time frame: up to 28 day
The relative of lncRNA NEAT1、miR-27b and Nrf2 with the time of mechanical ventilation, severity and mortality in 28 days of ARDS patients
Time frame: up to 28 day
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Jun 2021.
- Background: PubMed 22797452ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669.
- Background: PubMed 29466596Fan E, Brodie D, Slutsky AS. Acute Respiratory Distress Syndrome: Advances in Diagnosis and Treatment. JAMA. 2018 Feb 20;319(7):698-710. doi: 10.1001/jama.2017.21907.
- Background: PubMed 27192495Lu MC, Ji JA, Jiang ZY, You QD. The Keap1-Nrf2-ARE Pathway As a Potential Preventive and Therapeutic Target: An Update. Med Res Rev. 2016 Sep;36(5):924-63. doi: 10.1002/med.21396. Epub 2016 May 18.
- Background: PubMed 29684352Wei J, Chen G, Shi X, Zhou H, Liu M, Chen Y, Feng D, Zhang P, Wu L, Lv X. Nrf2 activation protects against intratracheal LPS induced mouse/murine acute respiratory distress syndrome by regulating macrophage polarization. Biochem Biophys Res Commun. 2018 Jun 7;500(3):790-796. doi: 10.1016/j.bbrc.2018.04.161. Epub 2018 Apr 25.
- Background: PubMed 29163554Liu Q, Lv H, Wen Z, Ci X, Peng L. Isoliquiritigenin Activates Nuclear Factor Erythroid-2 Related Factor 2 to Suppress the NOD-Like Receptor Protein 3 Inflammasome and Inhibits the NF-kappaB Pathway in Macrophages and in Acute Lung Injury. Front Immunol. 2017 Nov 9;8:1518. doi: 10.3389/fimmu.2017.01518. eCollection 2017.
- Background: PubMed 28486213Liu Y, Song M, Zhu G, Xi X, Li K, Wu C, Huang L. Corynoline attenuates LPS-induced acute lung injury in mice by activating Nrf2. Int Immunopharmacol. 2017 Jul;48:96-101. doi: 10.1016/j.intimp.2017.04.029. Epub 2017 May 6.
- Background: PubMed 26790856Rajasekaran S, Pattarayan D, Rajaguru P, Sudhakar Gandhi PS, Thimmulappa RK. MicroRNA Regulation of Acute Lung Injury and Acute Respiratory Distress Syndrome. J Cell Physiol. 2016 Oct;231(10):2097-106. doi: 10.1002/jcp.25316. Epub 2016 Feb 4.
- Background: PubMed 29727715Wu CT, Huang Y, Pei ZY, Xi X, Zhu GF. MicroRNA-326 aggravates acute lung injury in septic shock by mediating the NF-kappaB signaling pathway. Int J Biochem Cell Biol. 2018 Aug;101:1-11. doi: 10.1016/j.biocel.2018.04.019. Epub 2018 May 1.
- Background: PubMed 30121199Ling Y, Li ZZ, Zhang JF, Zheng XW, Lei ZQ, Chen RY, Feng JH. RETRACTED: MicroRNA-494 inhibition alleviates acute lung injury through Nrf2 signaling pathway via NQO1 in sepsis-associated acute respiratory distress syndrome. Life Sci. 2018 Oct 1;210:1-8. doi: 10.1016/j.lfs.2018.08.037. Epub 2018 Aug 17.
- Background: PubMed 28351320Ding L, Ni J, Yang F, Huang L, Deng H, Wu Y, Ding X, Tang J. Promising therapeutic role of miR-27b in tumor. Tumour Biol. 2017 Mar;39(3):1010428317691657. doi: 10.1177/1010428317691657.
- Background: PubMed 22615562Zhou R, Gong AY, Eischeid AN, Chen XM. miR-27b targets KSRP to coordinate TLR4-mediated epithelial defense against Cryptosporidium parvum infection. PLoS Pathog. 2012;8(5):e1002702. doi: 10.1371/journal.ppat.1002702. Epub 2012 May 17.
- Background: PubMed 26980776Signorelli SS, Volsi GL, Pitruzzella A, Fiore V, Mangiafico M, Vanella L, Parenti R, Rizzo M, Volti GL. Circulating miR-130a, miR-27b, and miR-210 in Patients With Peripheral Artery Disease and Their Potential Relationship With Oxidative Stress. Angiology. 2016 Nov;67(10):945-950. doi: 10.1177/0003319716638242. Epub 2016 Jul 11.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Acute Respiratory Distress Syndrome and Inflammation, run by Beijing Anzhen Hospital at 1 site in China.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 7 inclusion and 8 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 24 Jun 2021. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in China. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
The expression of lncRNA NEAT1 in blood and BALF in all groups (time frame: up to 24 day). The study lists 10 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT04937855, which also lists 19 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 24 Jun 2021.