ArticleBioscience reports2026
Serum proteomics mirrors the histopathological changes underlying different etiologies of primary mitral valve disease.
Article in Bioscience reports, 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
13 authors.
Funding
Abstract
Mitral valve disease (MVD) is the most common valvulopathy and a frequent cause of heart failure and death. However, data regarding the molecular basis are scarce. We aimed to thoroughly explore and compare the circulating, molecular, and histopathological profiles in the main subtypes of primary chronic MVD. In total, 300 patients with chronic primary MVD undergoing mitral valve (MV) replacement were enrolled and classified in the four main etiologic subtypes: calcific mitral valve disease (CMVD, n = 81), rheumatic disease (RHVD, n = 114), Barlow's disease (BD, n = 70), and fibroelastic deficiency (FED, n = 35). Discovery studies were performed using Olink Proteomics® technology in 80 serums from MVD patients (n = 20/etiology). Histopathologic study, ELISA, and zymography were performed on resected MVs to analyze extracellular matrix (ECM) composition and remodeling, inflammation, and calcification. Serum proteomics identified markers exclusively overexpressed in each MVD etiologic subtype. Further enrichment analyses revealed specific etiology-dependent pathways involving calcification, inflammation, or ECM remodeling. Such etiology-dependent differences were mirrored in the excised MVs both architecturally and compositionally. CMVD and RHVD valves had a marked ECM disorganization with increased collagen deposition and presence of nodular and diffuse calcification, respectively. Moreover, RHVD valves exhibited high levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and matrix degradation enzymes. BD valves showed enhanced inflammatory markers and infiltrates. Moreover, BD and FED valves presented marked proteoglycans deposition. Our study identified circulating markers involved in calcification, inflammation, and ECM remodeling, which may be associated with specific MVD etiologies. The differences in serum markers seem to mirror histopathologic and molecular alterations in the MVs with potential applications into the clinic as diagnosis biomarkers. Identification of underlying molecular mechanisms of each etiology is essential to discover new specific therapeutic targets.
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.