ReviewMolecular medicine (Cambridge, Mass.)2026
Hydrogen sulfide-mediated protein s-persulfidation: a regulatory mechanism in cardiovascular homeostasis.
Review in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 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
backgroundCardiovascular diseases represent a primary cause of global mortality. Hydrogen sulfide operates as a major endogenous gasotransmitter that contributes to cardiovascular homeostasis through multiple biochemical mechanisms, among which protein S-persulfidation, represents a major redox-sensitive post-translational mechanism. This dynamically reversible modification converts cysteine sulfhydryl groups into highly nucleophilic persulfide groups to prevent irreversible oxidative damage. AIM OF REVIEW: This review aims to systematically synthesize the current molecular understanding of S-persulfidation in cardiovascular biology. We evaluate the methodological evolution of site-specific detection technologies, delineate the regulatory mechanisms of sulfur signaling across distinct physiological axes, and assess the clinical translational potential of reactive sulfur species delivery systems. KEY SCIENTIFIC CONCEPTS OF REVIEW: The manuscript outlines the evolution of detection methodologies from early biotin-switch assays to Quantitative Thiol Reactivity Profiling. Mechanistically, S-persulfidation modulates membrane potential and vascular tone by altering the open probability of ion channels including K
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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.