ReviewAmerican journal of physiology. Lung cellular and molecular physiology2026
Mitochondrial-derived microproteins in lung disease: insights and implications.
Review in American journal of physiology. Lung cellular and molecular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Mitochondrial and Epigenetic Drivers of Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2026Review
- MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases.Journal of translational medicine · 2026Review
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
As bioactive microproteins, mitochondrial-derived microproteins (MDPs) are encoded within the small open reading frames of mitochondrial DNA. MDPs have been shown to be altered in a number of disease states and have mitochondrial, nuclear, and extracellular actions. Most published work on MDPs has focused on MOTS-c and Humanin's actions in tissues with high mitochondrial density (heart, skeletal muscle, and brain) or in disease states of advanced age-Alzheimer's, cancer, and cardiovascular disease. This review aims to highlight the existing gaps in knowledge related to MDPs' role in lung homeostasis and disease-including acute lung injury, chronic obstructive pulmonary disease, allergic asthma, and pulmonary fibrosis. The increasingly recognized role of MDPs in nonpulmonary diseases sheds light on the importance of more investigations of MDPs, their clinical and mechanistic roles, and their therapeutic potential for pulmonary diseases.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.