Human study PLS-00087
Reduced skeletal muscle expression of mitochondrial-derived peptides humanin and MOTS-C and Nrf2 in chronic kidney disease.
Version 1 · published November 7, 2026 · evidence through November 7, 2026 · research snapshot 2026.1.1 · methodology ev-1 · Automated assessment by AI (claude-opus-5-5 and claude-sonnet-5-5), not reviewed by a person.
Only the abstract was available. Essential methods may be missing, which limits what can be judged.
Reports of this study
Every publication, registration and abstract describing this one study. Participants are counted once.
- Reduced skeletal muscle expression of mitochondrial-derived peptides humanin and MOTS-C and Nrf2 in chronic kidney disease.primary · American journal of physiology. Renal physiology · 2019-08-21 · PMID 31432706 · DOI
Design and participants
- Design
- Cross-sectional study
- Population
- Patients with stage 5 chronic kidney disease and age-matched controls with normal renal function
- Conditions
- Chronic kidney disease stage 5
- Planned enrollment (registry)
- Not reported
- Enrolled
- Not reported
- Randomized
- Not reported
- Completed follow-up
- Not reported
Intervention and comparator
What each group received. Related peptides, analogs and combinations are never treated as the compound itself.
What the authors reported
As stated in the sources. This is the authors’ account, not Peptide Library’s assessment.
Adverse events
None reported. That is not evidence of safety, and how safety was monitored isn’t described.
The authors concluded (paraphrased): MOTS-c was reduced in muscle and serum in CKD, while humanin was raised in serum but reduced in muscle. Low muscle peptide levels were linked to lower mitochondrial density, oxidative stress and systemic inflammation, which are features of uremia and premature aging.
Peptide Library’s assessment
An automated assessment, made by AI separately from the authors’ conclusions and not reviewed by a person. How risk of bias is assessed.
Limitations
- other: MOTS-c was only measured as an endogenous peptide. It was not administered, so the study gives no evidence on the effects of the compound as an intervention.
- abstract only: Only the abstract is available. Sample sizes, methods and numerical results are not reported in the record.
- confounding: Cross-sectional comparison of CKD patients with controls. Associations with mitochondrial density and oxidative stress may be confounded.
- inappropriate population: The study measured endogenous peptide levels in CKD patients. No compound was administered, so it gives no intervention evidence.
No risk-of-bias assessment has been published for this study’s results.
Claims this study informs
- Improves metabolic health: not eligible (not primary study) for “Insulin sensitivity, glucose control or body weight”
- Is safe for human administration: not eligible (not primary study) for “Adverse events, serious adverse events and discontinuations”
Where each value comes from
- author_conclusion: PMID 31432706, abstract (sentences 8-9) · extracted by AI (automated, not verified by a person) · abstract only
- design: PMID 31432706, abstract (sentence 4) · extracted by AI (automated, not verified by a person) · abstract only
- population: PMID 31432706, abstract (sentence 4) · extracted by AI (automated, not verified by a person) · abstract only
Version 1 · published November 7, 2026 · evidence through November 7, 2026 · research snapshot 2026.1.1 · methodology ev-1 · Automated assessment by AI (claude-opus-5-5 and claude-sonnet-5-5), not reviewed by a person.
These assessments describe published research. Records marked automated were produced by AI under the published methodology and have not been reviewed by a person; they can contain errors. None of this is medical advice, not a statement about any product’s safety for human use, and not a regulatory approval. Peptide Library’s vendor and partner relationships play no part in them (editorial independence).