SepsisNCT05148117
Mitochondrial Dysfunction Contributes to Sepsis Induced Cardiac Dysfunction
An observational study of Sepsis, run by University of Alabama at Birmingham at 1 site in United States.
Trial summary
This proposal hypothesizes that mitochondrial bioenergetics in the patient will correspond to mtDNA DAMPs levels and markers of inflammation. We predict these will serve as a prognostic indicator of Sepsis induced cardiac dysfunction (SICD) outcomes. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Sepsis
- What is being tested?
- Suspected Sepsis Group - Diagnostic Measurements
- How many people
- 0 participants
- Where
- 1 siteUnited States
- Study dates
- 10 Dec 2025to 14 Jan 2026
- 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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: study patients admitted to the intensive care unit with suspected sepsis shock will be enrolled and compared to the control group.
Who may be able to join
- Subjects 18 years old
- With clinical symptoms suggestive of sepsis Control Group
- age matched
- gender matched
- cardiovascular risk factor matched
Who cannot join
- n/a
Trial locations and contacts
1 site in 1 country.
United States1 site
University of Alabama at Birmingham
Birmingham, Alabama, 35294
About this study
This proposal hypothesizes that mitochondrial bioenergetics in the patient will correspond to mtDNA DAMPs levels and markers of inflammation. We predict these will serve as a prognostic indicator of Sepsis induced cardiac dysfunction (SICD) outcomes. Successful completion of these studies will provide a clearer understanding of the etiology of SICD development and therefore will have a high impact on biomedical research by identifying a new mechanism for understanding sepsis induced organ failure. Importantly, they will also provide a means for more directed and focused therapies, based upon individual bioenergetic/mitochondrial-mediated inflammation profiles. The combined, complementary expertise of the Mentor/co-primary investigators (Drs. Mathru and Ballinger) provide an excellent combination in both basic and translational research. They also have experience conducting studies and publications that will strengthen this research project. Importantly, the methods for characterizing mitochondrial bioenergetics from platelets were developed here at UAB, and methods for quantitative assessment of mtDNA DAMPs have been recently developed.
Read the detailed description
Sepsis induced cardiac dysfunction (SICD) occurs in ~ 50% of the patients with severe sepsis and septic shock, with significant implications for patient's survival. Currently, the precise pathophysiological mechanisms leading to cardiac dysfunction are not fully understood, nor is there an effective therapy for SICD except antibiotics, source control and restoration of hemodynamics to improve organ perfusion.
SICD is characterized by minimal cell death, normal coronary perfusion, preserved tissue oxygen tension and reversibility in survivors. These characteristics point toward an oxygen utilization problem due to mitochondrial dysfunction; interestingly, sepsis mouse models demonstrated an improvement in cardiac function and decreased mortality when they were treated with mitochondrial targeted therapies, consistent with a growing body of evidence that suggests dysregulated mitochondrial metabolism plays a pivotal role in the pathogenesis of SICD. Ultrastructural and functional abnormalities of mitochondria have also been demonstrated in early sepsis, and reactive oxygen species (ROS) generated from mitochondria along with calcium overload trigger mitochondrial permeability transition pore (mPTP) opening which facilitates the externalization of mitochondrial DNA (mtDNA) fragments. These mtDNA fragments, or mtDNA Damage Associated Molecular Patterns (mtDNA DAMPs), activate innate immune response pathways - these pathways are well known to be significant components of intramyocardial inflammation.
- Conditions
- Sepsis
- Being tested
- Suspected Sepsis Group - Diagnostic Measurements, Control Group - Diagnostic Measurements
- Medical subject headings
- Sepsis
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Suspected Sepsis Group - Diagnostic MeasurementsDiagnostic test
Blood samples (7.5ml) will be collected in cell free DNA collection tubes cfDNA will be extracted with the use of MagMAX cell free DNA isolation kit. Quantitative PCR will determine the total cfDNA. cfDNA (5micro litr) will be subjected to bisulphide conversion with use of EZ DNA methylation kit (Zymo research). We will perform digital PCR for interrogating bisulphide treated cfDNA for FMA 101A locus with the use of Quant Studio 3D digital PCR system. Copy numbers of unmethylated FAM 101A locus as determined by d PCR in the sample will be expressed as the copy numbers of cardiomyocyte specific cfDNA per plasma volume.Inflammatory markers IL-6.IL-8, IL 1-18 and C-reactive protein (CRP) will be measured using commercial assays. Speckle tracking imaging will be used to obtain tissue displacement, velocity, strain, and strain rate in radial longitudinal and circumferential planes EF and FS will be determined by conventional methods.
Control Group - Diagnostic MeasurementsDiagnostic test
Blood samples (7.5ml) will be collected in cell free DNA collection tubes cfDNA will be extracted with the use of MagMAX cell free DNA isolation kit. Quantitative PCR will determine the total cfDNA. cfDNA (5micro litr) will be subjected to bisulphide conversion with use of EZ DNA methylation kit (Zymo research). We will perform digital PCR for interrogating bisulphide treated cfDNA for FMA 101A locus with the use of Quant Studio 3D digital PCR system. Copy numbers of unmethylated FAM 101A locus as determined by d PCR in the sample will be expressed as the copy numbers of cardiomyocyte specific cfDNA per plasma volume.Inflammatory markers IL-6.IL-8, IL 1-18 and C-reactive protein (CRP) will be measured using commercial assays. Speckle tracking imaging will be used to obtain tissue displacement, velocity, strain, and strain rate in radial longitudinal and circumferential planes EF and FS will be determined by conventional methods.
| Study group | Role | What they receive |
|---|---|---|
| suspected sepsis group | We will perform a prospective observational study of patients admitted to the intensive care units (ICU) with suspected sepsis or septic shock. Receives: Diagnostic Test: Suspected Sepsis Group - Diagnostic Measurements | |
| control group | This group will be compared to suspected sepsis or sepsis shock patients. The control group will be age matched, gender-matched, and cardiovascular risk-factor matched controls. Receives: Diagnostic Test: Control Group - Diagnostic Measurements |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mitochondrial dysfunction characterized by bioenergetic changes
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Measured: within 6 hours of admission to the ICU
Mitochondrial dysfunction characterized by bioenergetic changes
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Measured: within 72 hours post admission
Mitochondrial dysfunction characterized by bioenergetic changes
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Measured: after clinical recovery from sepsis (approximately 1 month)
Mitochondrial function in heart
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Measured: within 6 hours of admission to the ICU
Mitochondrial function in heart
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Measured: within 72 hours post admission
Mitochondrial function in heart
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Measured: after clinical recovery from sepsis (approximately 1 month)
Mitochondria and SICD
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Measured: within 6 hours of admission to the ICU
Mitochondria and SICD
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Measured: within 72 hours post admission
Mitochondria and SICD
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Measured: after clinical recovery from sepsis (approximately 1 month)
Mitochondrial mechanisms to influence SICD
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Measured: within 6 hours of admission to the ICU
Mitochondrial mechanisms to influence SICD
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Measured: within 72 hours post admission
Mitochondrial mechanisms to influence SICD
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Measured: after clinical recovery from sepsis (approximately 1 month)
Mitochondrial bioenergetics and mtDNA DAMPs
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Measured: within 6 hours of admission to the ICU
Mitochondrial bioenergetics and mtDNA DAMPs
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Measured: within 72 hours post admission
Mitochondrial bioenergetics and mtDNA DAMPs
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Measured: after clinical recovery from sepsis (approximately 1 month)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Dec 2021
- Study start10 Dec 2025
- Primary completion14 Jan 2026
- Study completion14 Jan 2026
Why it stopped: Could not get through IRB submission and co-investigators with needed skillsets for study departed organization
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for SepsisStudies of the same condition, open and under way.
- More trials run by University of Alabama at BirminghamThe 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
- Case-control
- Time perspective
- Prospective
- Enrolment
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Alabama at Birmingham
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Riaz Karukappadath, University of Alabama at Birmingham
- Investigators
- Riaz Karukappadath, MD, Principal investigator, Department of Anesthesiology and Perioperative Medicine, Division of Critical Care Medicine
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05148117
- Sponsor's protocol ID
- 300007609
- Other IDs
- UAB
- Status last verified
- Feb 2026
- First submitted
- 24 Nov 2021
- Last updated
- 20 Feb 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: To be determined
Study at a glance
From the registry record, last updated by the sponsor on 20 Feb 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Mitochondrial Dysfunction Contributes to Sepsis Induced Cardiac Dysfunction
- ClinicalTrials.gov ID
- NCT05148117
- Acronym / sponsor ID
- 300007609
- Conditions
- Sepsis
- Study type
- Observational
- Recruitment status
- WithdrawnReason stopped: Could not get through IRB submission and co-investigators with needed skillsets for study departed organization
- Enrolment
- 0 participants (actual)
- Lead sponsor
- University of Alabama at BirminghamUniversity, hospital or other
- Study start
- 10 Dec 2025 (actual)
- Primary completion
- 14 Jan 2026 (actual)
- Study completion
- 14 Jan 2026 (actual)
- First posted
- 8 Dec 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.
This proposal hypothesizes that mitochondrial bioenergetics in the patient will correspond to mtDNA DAMPs levels and markers of inflammation. We predict these will serve as a prognostic indicator of Sepsis induced cardiac dysfunction (SICD) outcomes. Successful completion of these studies will provide a clearer understanding of the etiology of SICD development and therefore will have a high impact on biomedical research by identifying a new mechanism for understanding sepsis induced organ failure. Importantly, they will also provide a means for more directed and focused therapies, based upon individual bioenergetic/mitochondrial-mediated inflammation profiles. The combined, complementary expertise of the Mentor/co-primary investigators (Drs. Mathru and Ballinger) provide an excellent combination in both basic and translational research. They also have experience conducting studies and publications that will strengthen this research project. Importantly, the methods for characterizing mitochondrial bioenergetics from platelets were developed here at UAB, and methods for quantitative assessment of mtDNA DAMPs have been recently developed.
Detailed description
Sepsis induced cardiac dysfunction (SICD) occurs in ~ 50% of the patients with severe sepsis and septic shock, with significant implications for patient's survival. Currently, the precise pathophysiological mechanisms leading to cardiac dysfunction are not fully understood, nor is there an effective therapy for SICD except antibiotics, source control and restoration of hemodynamics to improve organ perfusion.
SICD is characterized by minimal cell death, normal coronary perfusion, preserved tissue oxygen tension and reversibility in survivors. These characteristics point toward an oxygen utilization problem due to mitochondrial dysfunction; interestingly, sepsis mouse models demonstrated an improvement in cardiac function and decreased mortality when they were treated with mitochondrial targeted therapies, consistent with a growing body of evidence that suggests dysregulated mitochondrial metabolism plays a pivotal role in the pathogenesis of SICD. Ultrastructural and functional abnormalities of mitochondria have also been demonstrated in early sepsis, and reactive oxygen species (ROS) generated from mitochondria along with calcium overload trigger mitochondrial permeability transition pore (mPTP) opening which facilitates the externalization of mitochondrial DNA (mtDNA) fragments. These mtDNA fragments, or mtDNA Damage Associated Molecular Patterns (mtDNA DAMPs), activate innate immune response pathways - these pathways are well known to be significant components of intramyocardial inflammation.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| suspected sepsis group | – | Diagnostic Test: Suspected Sepsis Group - Diagnostic MeasurementsWe will perform a prospective observational study of patients admitted to the intensive care units (ICU) with suspected sepsis or septic shock. |
| control group | – | Diagnostic Test: Control Group - Diagnostic MeasurementsThis group will be compared to suspected sepsis or sepsis shock patients. The control group will be age matched, gender-matched, and cardiovascular risk-factor matched controls. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- study patients admitted to the intensive care unit with suspected sepsis shock will be enrolled and compared to the control group.
Key inclusion criteria (5 listed)
- Subjects 18 years old
- With clinical symptoms suggestive of sepsis Control Group
- age matched
- gender matched
- cardiovascular risk factor matched
Key exclusion criteria (1 listed)
- n/a
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 |
|---|---|---|
| Suspected Sepsis Group - Diagnostic MeasurementsBlood samples (7.5ml) will be collected in cell free DNA collection tubes cfDNA will be extracted with the use of MagMAX cell free DNA isolation kit. Quantitative PCR will determine the total cfDNA. cfDNA (5micro litr) will be subjected to bisulphide conversion with use of EZ DNA methylation kit (Zymo research). We will perform digital PCR for interrogating bisulphide treated cfDNA for FMA 101A locus with the use of Quant Studio 3D digital PCR system. Copy numbers of unmethylated FAM 101A locus as determined by d PCR in the sample will be expressed as the copy numbers of cardiomyocyte specific cfDNA per plasma volume.Inflammatory markers IL-6.IL-8, IL 1-18 and C-reactive protein (CRP) will be measured using commercial assays. Speckle tracking imaging will be used to obtain tissue displacement, velocity, strain, and strain rate in radial longitudinal and circumferential planes EF and FS will be determined by conventional methods. | Diagnostic test | suspected sepsis group |
| Control Group - Diagnostic MeasurementsBlood samples (7.5ml) will be collected in cell free DNA collection tubes cfDNA will be extracted with the use of MagMAX cell free DNA isolation kit. Quantitative PCR will determine the total cfDNA. cfDNA (5micro litr) will be subjected to bisulphide conversion with use of EZ DNA methylation kit (Zymo research). We will perform digital PCR for interrogating bisulphide treated cfDNA for FMA 101A locus with the use of Quant Studio 3D digital PCR system. Copy numbers of unmethylated FAM 101A locus as determined by d PCR in the sample will be expressed as the copy numbers of cardiomyocyte specific cfDNA per plasma volume.Inflammatory markers IL-6.IL-8, IL 1-18 and C-reactive protein (CRP) will be measured using commercial assays. Speckle tracking imaging will be used to obtain tissue displacement, velocity, strain, and strain rate in radial longitudinal and circumferential planes EF and FS will be determined by conventional methods. | Diagnostic test | control group |
Primary outcome
Mitochondrial dysfunction characterized by bioenergetic changes
Time frame: within 6 hours of admission to the ICU
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Mitochondrial dysfunction characterized by bioenergetic changes
Time frame: within 72 hours post admission
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Mitochondrial dysfunction characterized by bioenergetic changes
Time frame: after clinical recovery from sepsis (approximately 1 month)
that mitochondrial dysfunction, characterized by bioenergetic changes (dysfunction) is associated with sepsis in humans, and will be significantly linked with mtDNA DAMPs levels and inflammatory markers in the pathophysiology of SICD.
Mitochondrial function in heart
Time frame: within 6 hours of admission to the ICU
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Mitochondrial function in heart
Time frame: within 72 hours post admission
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Mitochondrial function in heart
Time frame: after clinical recovery from sepsis (approximately 1 month)
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation
Mitochondria and SICD
Time frame: within 6 hours of admission to the ICU
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Mitochondria and SICD
Time frame: within 72 hours post admission
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Mitochondria and SICD
Time frame: after clinical recovery from sepsis (approximately 1 month)
examining the potential roles for increased reactive oxygen species (ROS) and nitric oxide (NO) production in SICD using mouse models of sepsis have shown that genetic and/or pharmacologic manipulation of these species decreased oxidative stress, increased ATP generation and restored cardiac function in sepsis
Mitochondrial mechanisms to influence SICD
Time frame: within 6 hours of admission to the ICU
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Mitochondrial mechanisms to influence SICD
Time frame: within 72 hours post admission
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Mitochondrial mechanisms to influence SICD
Time frame: after clinical recovery from sepsis (approximately 1 month)
changes in mitochondrial bioenergetics associated with sepsis can result in differential releases of mtDNA DAMPs, which contribute in inflammation.
Mitochondrial bioenergetics and mtDNA DAMPs
Time frame: within 6 hours of admission to the ICU
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Mitochondrial bioenergetics and mtDNA DAMPs
Time frame: within 72 hours post admission
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Mitochondrial bioenergetics and mtDNA DAMPs
Time frame: after clinical recovery from sepsis (approximately 1 month)
determine the mitochondrial bioenergetic profiles from platelets isolated from blood samples collected from sepsis patients and controls.
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 20 Feb 2026.
- Individual participant dataSharing planned: No. To be determined
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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.
Riaz Karukappadath, MD principal investigator
Department of Anesthesiology and Perioperative Medicine, Division of Critical Care Medicine
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 Sepsis, run by University of Alabama at Birmingham at 1 site in United States.
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 5 inclusion and 1 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: withdrawn, as of the sponsor's last update on 20 Feb 2026. 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 United States. 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?
The study was withdrawn before enrolling participants, so there are no results.
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?
Mitochondrial dysfunction characterized by bioenergetic changes (time frame: within 6 hours of admission to the ICU). The study lists 15 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
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 20 Feb 2026.