ArticleJournal of translational medicine2026
Harnessing the novel safeguarding role of Selenoprotein T in age-related myocardial left and right decline through the ferroptosis-mitochondrial axis.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
backgroundCardiovascular aging critically increases myocardial susceptibility to ischemia/reperfusion (I/R) injury. Selenoprotein T (SELENOT) has emerged as a novel modulator of cardiomyocyte differentiation and protection. However, its involvement in chronic age-associated cardiac dysfunction is unknown.
methodsUsing a D-galactose ageing model in which cardiac impairment was worsened by I/R injury, combined with histological, cellular, and molecular analyses, we investigated the cardioprotective potential of a small SELENOT mimetic peptide (PSELT).
resultsPSELT improved basal and post-ischemic left and right ventricular (LV and RV) hemodynamics, preserved myocardial architecture, and attenuated fibrosis and myofibrillar disorganization. Consistent with its ability to lower baseline RV workload, PSELT diminished pulmonary inflammation and fibrosis. Cardioprotection was further supported by decreased coronary LDH leakage and infarct size. Mechanistically, PSELT downregulated senescence markers (p21, p16), preserved desmin and SERCA2a expression, and attenuated inflammation by reducing NLRP3, caspase-1, and NF-κB nuclear translocation in aged LV and RV. PSELT counteracted cardiac ferroptosis by preserving GPX4 levels, limiting ACSL4 expression, and reducing lipid peroxidation and Fe2+ levels, while mitigating ferroptotic death in RSL3-stimulated senescent cardiomyocytes. Additionally, PSELT normalized mitochondrial dynamics restoring DRP1, mitofusin-2 and OPA1 expression in cardiac mitochondria, while reducing Ca²⁺-induced mitochondrial swelling and mPTP opening. In human senescent cardiomyocytes, PSELT decreased p21 and p16, lowered SA-β-gal activity, improved mitochondrial membrane potential, enhanced respiration, and increased OCR and ECAR, while mitigating aging-related SELENOT overexpression.
conclusionsPSELT enhances LV and RV resistance to I/R injury in aged hearts through the ferroptosis-mitochondrial axis and supports its potential as a therapeutic strategy against age-associated cardiac dysfunction.
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.