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Journal articleYin S, Mayr U, Barallobre-Barreiro J, et al., 2026,
Aortic Stenosis Hyalectan Remodeling Revealed by Proteomics and Glycoproteomics.
, Arterioscler Thromb Vasc Biol, Vol: 46BACKGROUND: Calcific aortic valve (AV) disease (CAVD) is recognized as an active pathological process involving extracellular matrix remodeling. This study investigates extracellular matrix remodeling through proteomic analysis and a novel mouse model of aortic stenosis. METHODS: Proteomic and glycoproteomic analyses were conducted on AV leaflets from heart transplant donors (n=29) and patients with CAVD (n=17). Each CAVD sample was subdivided into noncalcified and calcified regions. To investigate the functional impact of extracellular matrix remodeling on aortic stenosis, we crossed apolipoprotein E-deficient mice (ApoE-/-) with mice lacking the catalytic domain of ADAMTS5 (Adamts5Δcat) to generate a mouse model combining hyalectan accumulation with hypercholesterolemia. RESULTS: Proteomic and glycoproteomic analyses revealed hyalectan accumulation in CAVD compared with control valves. Versican predominated in noncalcified regions, while aggrecan was enriched in calcified regions. The shift in hyalectan composition correlated with changes in AV pressure gradient, elevated osteoblast-like cell markers, and inflammatory proteins, most notably pentraxin 3. Both versican and aggrecan are characterized by their ability to bind hyaluronan and serve as substrates of ADAMTS5. In Adamts5Δcat/ApoE-/- mice, hyalectan accumulation was associated with narrowed aortic cusp separation and increased post-AV velocity. Proteomic analysis of AVs from Adamts5Δcat/ApoE-/- mice revealed elevated versican, aggrecan, and pentraxin 3, recapitulating key features of human CAVD. Single-cell RNA sequencing and in vitro experiments linked versican to activated valve interstitial cells, while aggrecan colocalized with calcification markers in osteoblast-like cells. Pentraxin 3 was bound to hyaluronan and accumulated in calcified AVs. ADAMTS5 deficiency was sufficient to cause intact versican accumulation and promote valve interstitial cell activation, accompanied by increased
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Journal articleTakov K, Penkov S, Pechlaner R, et al., 2026,
Lipoprotein(a) carries triglyceride species associated with incident cardiovascular disease.
, Atherosclerosis, Vol: 420BACKGROUND AND AIMS: Lipoprotein(a) [Lp(a)] is described as a low-density lipoprotein-like particle, but recent work suggests heterogeneity, including triglyceride (TG)-rich features. We investigated whether native Lp(a) carries an apolipoprotein E (APOE)-associated TG signature, whether it is remodeled postprandially, and whether Lp(a)-associated TG species are linked to cardiovascular risk. METHODS: Plasma Lp(a) was immunocaptured under native conditions and analyzed by proteomics in patients with high Lp(a) (n = 15) and lipidomics in healthy volunteers (n = 9). Lp(a) produced in HepG2 cells was characterized using immunoprecipitation, density gradient ultracentrifugation, microsomal triglyceride transfer protein inhibition, and fatty acid loading. Matched fasting and postprandial samples assessed Lp(a) lipidome remodeling (n = 6). The relationship between Lp(a)-associated TGs and cardiovascular risk was examined in the community-based Bruneck Study (n = 623). RESULTS: Direct plasma Lp(a) immunocapture showed APOE enrichment, confirmed by proteomics, immunoblotting, reverse APOE immunocapture, and size-exclusion chromatography followed by Lp(a) immunoprecipitation. In vitro, HepG2 cells secreted APOE-containing Lp(a) that was more buoyant than apolipoprotein B (APOB)-only particles and less affected by lomitapide or fatty acid loading. The Lp(a) lipidome was more stable postprandially than plasma lipids. Plasma Lp(a) depletion reduced 35 lipid species, predominantly TGs, including TG(52:3) and TG(52:4), previously linked to incident cardiovascular disease. TG reduction following Lp(a) depletion correlated with attenuation of cardiovascular risk after Lp(a) adjustment in the Bruneck Study, supporting a clinically relevant TG signature of native Lp(a). CONCLUSIONS: Native plasma Lp(a) carries a defined TG signature that is relatively stable postprandially and linked to incident cardiovascular disease.
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Journal articleMacko A, Pecon-Slattery J, Shovlin CL, 2026,
Translating evolutionary history and protein-focused machine learning supports increased prevalence of hereditary haemorrhagic telangiectasia, one of the most common inherited disorders
, QJM: An International Journal of Medicine, ISSN: 1460-2725<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>Recent genetic data suggest hereditary haemorrhagic telangiectasia (HHT) is 2-12 times more common than the clinically-ascertained prevalence, potentially above the ‘rare disease’ designation threshold, and undermining clinical predictions for asymptomatic individuals diagnosed by genetic testing.</jats:p> </jats:sec> <jats:sec> <jats:title>Aim</jats:title> <jats:p>To test, we examined if missense variants in HHT disease-causing genes may have been misclassified as pathogenic (LP/P) or benign (B/LB).</jats:p> </jats:sec> <jats:sec> <jats:title>Design</jats:title> <jats:p>Evaluation of ClinVar-annotated missense variants in ENG, ACVRL1 and SMAD4.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Human-independent methods using CodeXome for pan-primate evolutionary history, and AlphaMissense which incorporates AlphaFold predictions for protein misfolding were used to validate/reclassify pathogenic and benign missense variants</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>ClinVar annotations were commonly conservative with 35-90% of rare missense substitutions in ENG, ACVRL1 and SMAD4 classified as variants of uncertain significance (VUS). CodeXome identified 92% of ClinVar-annotated B/LB variants were shared with other primate species, supporting their benign classification. AlphaMissense metrics strongly c
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Journal articleMoss BAS, Duregotti E, Yin X, et al., 2026,
Generation of Fibrin-Based Three-Dimensional Engineered Vascular Tissues from Human Aortic Smooth Muscle Cells for Proteomic Analysis.
, J Vis ExpVascular smooth muscle cells (SMCs) reside within the medial layer of blood vessels, where they interact with an extracellular matrix (ECM) composed of collagen, elastin, and proteoglycans to maintain vascular structure and function. Aberrant ECM remodeling contributes to multiple vascular diseases; however, conventional two-dimensional culture systems do not adequately recapitulate the three-dimensional (3D) cellular and matrix environment required to study SMC-ECM interactions and matrix remodeling. This protocol describes the generation of engineered vascular tissues (EVTs) from primary human aortic SMCs cultured within fibrin-based 3D hydrogels. Following casting between flexible polydimethylsiloxane posts, EVTs undergo cellular alignment, contraction, and deposit de novo ECM, providing a physiologically relevant platform for studying vascular matrix biology. The protocol details tissue fabrication, culture, harvesting, and downstream analysis of newly deposited ECM by immunofluorescence staining. In addition, a workflow is presented for qualitative and quantitative characterization of EVT-derived proteins using Western blotting and mass spectrometry-based proteomics. Sequential protein extraction enables assessment of soluble and ECM-enriched protein fractions, facilitating in-depth evaluation of ECM composition. This platform provides a reproducible approach for investigating ECM production and remodeling by human SMCs in a 3D environment.
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Journal articleSingh B, Mayr M, 2026,
Decoding Plaque Instability Through Plasma Proteomics Profiling?
, JACC Basic Transl Sci, Vol: 11 -
Journal articleKhawaja SA, Hanna L, Singh A, et al., 2026,
A randomised trial of carbon dioxide flushing to reduce vascular brain injury in patients undergoing TAVI.
, EuroIntervention, Vol: 22, Pages: 883-890BACKGROUND: Stroke remains a significant concern in patients undergoing transcatheter aortic valve implantation (TAVI). Despite advances in TAVI technology and techniques, stroke rates have remained unchanged, with trials of cerebral embolic protection devices failing to reduce rates. The concept of air emboli has not been previously investigated in TAVI procedures. We hypothesised that gaseous emboli could play a significant role in TAVI and that carbon dioxide (CO2) flushing of the TAVI valves could reduce the incidence of new neurological lesions post-TAVI. AIMS: We aimed to demonstrate the neuroprotective benefits of CO2 flushing in TAVI patients. METHODS: INTERCEPTavi is a single-centre, blinded, randomised controlled pilot trial that studied the effects of flushing TAVI valves with CO2 versus conventional saline on neurological outcomes post-TAVI, assessed using magnetic resonance imaging (MRI) and transcranial Doppler (TCD). Patients with aortic stenosis were randomised after obtaining vascular access. Periprocedural TCD assessed solid and gaseous emboli to the brain. Post-procedure, patients underwent brain MRI to detect lesions. Here, we report the primary outcome of feasibility, as well as the secondary MRI and mechanistic TCD outcomes. RESULTS: A total of 60 patients were recruited and randomised 1:1 to CO2 and saline flushing (TAVI-CO2) versus saline flushing only (TAVI-S). CO2 flushing significantly reduced the average number of lesions per patient (TAVI-CO2: 4 lesions/patient vs TAVI-S: 8.5 lesions/patient; p=0.031). The total infarct area was numerically lower in the TAVI-CO2 group (40.32 mm2 vs 93.20 mm2), although this did not reach statistical significance (p=0.111). Similarly, TCD showed fewer microembolic signals in the TAVI-CO2 arm, primarily due to a reduction in gaseous emboli, but this difference was not statistically significant (p=0.5). CONCLUSIONS: INTERCEPTavi is a pioneering, first-in-human randomised trial that demonstrated that CO2 flu
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Journal articleWang D, Lawrie A, Delgado San Martin J, 2026,
Pre-diagnostic comorbidity pathways are associated with the timing of pulmonary hypertension outcomes: a case control study
, BMC Pulmonary Medicine, ISSN: 1471-2466Background: Pulmonary hypertension (PH) is a life-threatening condition often diagnosed late due to non-specific symptoms and overlapping comorbidities with other cardiovascular and respiratory diseases. Although there have been advances in treatment, diagnostic delays are common, and patients are treated late in their disease course. Investigating the temporal ordering of recorded comorbidities may provide insight into diagnostic patterns associated with delayed PH recognition and adverse outcomes. Methods: We identified 2,727 PH patients from the UK Biobank cohort of 440,014 participants with diseases diagnoses, and sampled two demographics-matched cohorts of chronic obstructive pulmonary disease (COPD) and heart failure (HF) with the same number of patients as the PH cohort but were not diagnosed with PH. Employing process mining, a methodology originating from business process analysis to extract temporal patterns from event logs, the temporal diagnostic sequences of comorbidity combinations preceding PH diagnosis were compared to those sequences in patients who received a final diagnosis COPD or HF. We also assessed the relative risk of mortality given different combinations of comorbidities and the genetic correlation between comorbidities. Results: Patients diagnosed with PH had prior diagnoses of hypertension (58.1%), atrial fibrillation (31.2%), and heart failure (43.2%). Process mining revealed that the temporal order of cardiometabolic comorbidities influences the timing to diagnosis of PH, COPD and HF. Patients in which type 2 diabetes was diagnosed before systemic hypertension had received PH diagnosis 2 years and 9 months faster than the reverse sequence, where hypertension preceded diabetes. For patients with a final diagnosis of PH, HF and COPD, diagnostic sequences in which hypercholesterolemia was recorded before systemic hypertension and type 2 diabetes were associated with shorter median intervals to PH diagnosis. A sequence involving diabetes, h
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Journal articleAkhundova N, Paul R, Fletcher B, et al., 2026,
Pre-surgical miR-675-5p associates with the inflammatory response to surgery and increases inflammatory gene expression in vitro
, Journal of Cachexia, Sarcopenia and Muscle, ISSN: 2190-5991Background A loss of muscle mass and strength is a marker of poor outcomes following surgery. Changes in muscle gene expression following surgery are likely to contribute to post-surgical muscle loss, but the mechanisms controlling these changes are not known. We have previously shown that miRNAs associate with muscle loss in disease, including surgery, so may contribute to changes in gene expression. We analysed the change in muscle gene expression following surgery and compared it to pre- and post-surgical miRNA expression. We then analysed the effect of one of these miRNAs (miR-675-5p) on gene expression in myoblasts in the presence and absence of an inflammatory stimulus. Methods Differential gene expression analysis was performed on RNAseq data from rectus femoris biopsies (n=18 male patients) pre- and post-surgery. Gene expression was compared with miRNA expression in the same samples to identify patterns of mRNA expression associated with physiology and miRNA expression. The effect of miR-675-5p on gene expression in the presence and absence of TNF-a was determined in LHCN myoblasts by RNAseq. Results Post-surgery muscle had increased expression of gene sets associated with TNF-a signalling (2.7fold) and MYC targets (2.7-fold). Loss of muscle mass and strength associated with MYC target gene sets, but inflammatory gene sets only associated with loss of strength. Comparing miRNA expression with post-surgery gene expression showed that pre-surgery miR675-5p expression was most closely associated with post-surgical gene expression, indicating that the pre-surgery phenotype is important in determining the response to surgery. Pre-surgery miR675-5p correlated with change in gene expression in response to surgery (b=1.30, p<0.001), such that individuals with the highest pre-surgery miR-675-5p had the largest change in gene expression in response to surgery. In LHCN myoblasts miR-675-5p increased CCL2 protein release approximately 1.5-fold (p<0.001). RNAs
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Journal articleSharma T, Fall T, Sayols-Baixeras S, et al., 2026,
Linking Lipidomics to Vulnerable Coronary Plaques: A PROSPECT II Substudy.
, Arterioscler Thromb Vasc Biol, Vol: 46BACKGROUND: Lipidomics, the comprehensive profiling of circulating lipid species, has emerged as a powerful tool to investigate metabolic alterations underlying coronary atherosclerosis. Understanding the mechanisms driving high-risk vulnerable plaque formation and progression to myocardial infarction remains a key therapeutic priority. This study investigates associations between circulating lipid metabolites and imaging-defined features of vulnerable coronary plaque. METHODS: Following revascularization, patients with myocardial infarction underwent 3-vessel coronary artery imaging with near-infrared spectroscopy and intravascular ultrasound to assess nonflow-limiting plaques for lipid core burden index and plaque burden. Multivariable models evaluated associations between 424 lipid metabolites in plasma, quantified by mass spectrometry, pan-coronary lipid, pan-coronary plaque burden, and high-risk vulnerable plaque measures (maximum lipid core burden index within any 4-mm segment across the entire lesion ≥324.7 and/or plaque burden ≥70%) in 877 patients. Findings were validated in the SCAPIS study (Swedish Cardiopulmonary Bioimage Study) using coronary computed tomography angiography-based measures of coronary artery calcium score and segment involvement score. RESULTS: We identified 156 significant associations (P<0.05) between lipid metabolites and coronary plaque characteristics across 39 metabolic pathways. Sphingomyelins were inversely associated with all plaque metrics, and 1-palmitoyl-2-oleoyl-GPE (glycero-3-phosphoethanolamine; 16:0/18:1), a phosphatidylethanolamine, was positively associated with all plaque metrics. After correcting for multiple testing, 27 lipid species across 7 pathways remained significant (q<0.05). The majority were linked to pan-coronary lipid burden, with the strongest inverse association observed for sphingomyelin d18:1/22:1, d18:2/22:0, and d16:1/24:1. Similar inverse patterns were seen for select dihydrosphingomyelin
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Journal articleZiverec A, Grangy J, Pécheux Y, et al., 2026,
Triple-helical ligands for collagen-binding proteins improve cartilage extracellular matrix production in nasal chondrocytes.
, Mater Today Bio, Vol: 39The use of articular chondrocytes for cartilage repair is constrained by donor-site morbidity, poor proliferation, and difficulties to maintain a stable phenotype. As a result, nasal chondrocytes (NCs) have recently emerged as an alternative cell source. To better establish the potential of NCs in tissue engineering, we have explored their response to the activation of collagen-binding proteins (integrins, discoidin domain receptors (DDRs) andthe secreted protein acidic cysteine-rich (SPARC)) which are essential to cartilage homeostasis. Ligands for these proteins were synthesized as triple-helical peptides (THPs) that mimic the biological and structural properties of collagen, and were covalently linked to PEG or alginate hydrogels hosting human NCs. Compared to human adipose-tissue mesenchymal stem cells, NCs over-expressed chondrogenic markers, yielding higher Sox9 translocation and type II collagen production. THP ligands significantly improved the expression of key cartilage extracellular matrix components in hydrogels, at both the RNA and protein level, for up to 21 days of culture. In particular, THP ligands for DDRs and SPARC led to increased glycosaminoglycan and collagen deposition. In addition, THPs limited fibrocartilage formation, matrix metalloproteinase 13 expression and chondrocytes hypertrophy after 7 days of culture in hydrogels. This work introduces a biomimetic strategy to drive the early stages of the formation of an engineered cartilage tissue from NCs, by replicating key cell/collagen interactions. It provides a preliminary effort to combine an accessible cell source with functionalized biomaterials for cartilage repair.
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Journal articleSchmiedmayer P, Johnson A, Schuetz N, et al., 2026,
Design and rationale of the my heart counts cardiovascular health study: a large-scale, fully digital biobank, and randomized trial of large language model-driven coaching of physical activity.
, Am J Prev Cardiol, Vol: 28BACKGROUND: Cardiovascular disease remains the leading cause of global morbidity and mortality. The original My Heart Counts smartphone application demonstrated the feasibility of large-scale, fully digital recruitment and trial conduct, but was limited by platform exclusivity and the need for human experts to create text-based behavioral interventions. METHODS: The next-generation My Heart Counts smartphone application is a prospective, observational cohort study with an embedded randomized crossover trial, evaluating personalized text-based coaching prompts, available in both English and Spanish. All study and trial operations will be conducted via the My Heart Counts smartphone application, re-designed using the open-source Stanford Spezi framework to support iOS, with a planned Android release in 2027. The target enrollment is N = 15,000 adults across the United States and United Kingdom. The study establishes a comprehensive digital biobank by synthesizing passive mobile health data (steps, flights climbed, heart rate, sleep, workouts), raw sensor data (e.g., accelerometry), longitudinal clinical surveys, active tasks (6-minute walk test and 12-minute Cooper run test), electrocardiograms (ECG), and electronic health record (EHR) data integrated via HL7 FHIR protocols. The embedded trial evaluates the effect of text-based coaching prompts generated by a large language model (LLM) grounded in the Transtheoretical Model of Change on daily physical activity, as compared to generic prompts. PLANNED ANALYSIS: The primary endpoint of the randomized crossover trial is change in daily step count between LLM-driven and generic text-based intervention arms, analyzed using mixed-effects models. Secondary endpoints include change in mean active minutes and calorie burn over each intervention week. Other exploratory analyses include the changes in submaximal (6-minute walk test) and maximal (Cooper 12-minute run test) cardiorespiratory fitness, changes to sensor-derived biom
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Journal articlePruktanakul T, Lynham S, Chen H, et al., 2026,
ComparativeAnalysis of Data Processing Tools forMass Spectrometry Proteomics in Cardiovascular Research
, Journal of Proteome Research, ISSN: 1535-3893<jats:title>Abstract</jats:title> <jats:p>Mass spectrometry-based proteomics requires advanced data processing tools, yet most comparative studies have relied on noncardiovascular data sets or standard protein mixtures, limiting their relevance to cardiovascular research. We systematically compared three label-free data-dependent acquisition (DDA) tools (FragPipe, MaxQuant, and Proteome Discoverer) and five data-independent acquisition (DIA) tools (DIA-NN, DIA-Umpire, MSFragger-DIA, MaxDIA, and Spectronaut) using real-world cardiovascular tissue and blood-derived proteomics data sets. FragPipe and Spectronaut generally achieved the greatest quantitative proteome coverage among the evaluated DDA and DIA tools, respectively, particularly in cardiovascular tissue data sets, although tool rankings varied across sample types and proteome subsets. Despite differences in identification and quantification performance, peptide physicochemical characteristics were broadly similar across tools. Integration of complementary differential expression outputs increased differentially expressed protein detection in several data sets while maintaining agreement with the main results. These findings provide practical guidance for selecting data processing tools in cardiovascular proteomics and support the use of integrative approaches to maximize biological information from proteomics data sets.</jats:p>
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Journal articleNaghavi N, Barbaro L, Griffiths M, et al., 2026,
Development of a hemolysis filter system for the selective removal of free hemoglobin, heme and iron from blood envisaged for use in extracorporeal circuits
, Scientific Reports, ISSN: 2045-2322Hemolysis, the rupture of red blood cells, releases hemoglobin, haem, and redox-active iron into the bloodstream. When the body’s scavenging capacity is overwhelmed, these species can exert deleterious effects, as seen in hemolytic disorders. Hemolysis can also occur in extracorporeal circuits due to mechanical forces acting on blood during circulation. To mitigate these effects, we developed a filter designed for integration into extracorporeal circuits that is designed to capture hemolysis-associated byproducts using immobilised ligands. The filter prototype comprises glyoxal-functionalized agarose beads covalently immobilized with three binding agents: haptoglobin (Hp, binds cell-free hemoglobin [cfHb]), human serum albumin (HSA, binds haem), and desferrioxamine (DFO, binds free iron). Ligand immobilization was optimized to achieve strong covalent attachment to the agarose matrix. Optimized immobilization produced high ligand loading per milliliter of beads (mean ± SD): Hp 74.4 ± 11.7 mg/mL, HSA 84.6 ± 8.2 mg/mL, and DFO 43.3 ± 4.8 mg/mL. In vitro studies showed removal capacities of 12.7 ± 0.2 mg/mL for cfHb, 2708.5 ± 18.5 µg/mL for haem, and 309.7 ± 13.7 µg/mL for iron. The system retained binding activity in plasma and hemolyzed whole blood, and no increase in TAT or D-dimer was detected under the tested ex vivo conditions. These findings demonstrate the potential of this affinity-based filtration system to reduce hemolysis-associated complications in extracorporeal circulation.
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Journal articleYogeswaran A, Fünderich M, Wendlandt K, et al., 2026,
Angiotensin Converting Enzyme Inhibition and Mortality in Pulmonary Hypertension Associated With Chronic Obstructive Pulmonary Disease (PH-COPD)
, Pulmonary Circulation, Vol: 16, ISSN: 2045-8932In 567 PH-COPD patients from the PVRI GoDeep Meta-Registry, ACE inhibitor use was associated with improved survival only in severe PH (PVR > 5 WU), supporting prospective trials targeting this high-risk subgroup.
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Journal articleKardys I, Mayr M, Mair J, et al., 2026,
Proteomics profiling for cardiovascular risk prediction: transforming clinical care.
, Eur Heart J Acute Cardiovasc Care, Vol: 15, Pages: 481-483 -
Journal articleIssitt T, Kagugbe GW, Toe QK, et al., 2026,
Iron Compartmentalisation and Vascular Endothelial Cell Dysfunction.
, Antioxidants (Basel), Vol: 15, ISSN: 2076-3921Iron is essential for life, but its safe use by the body depends on it being kept within tightly controlled compartments. When this compartmentalisation is disrupted-through haemolysis, saturation of scavenger proteins, or dysregulation of the hepcidin-ferroportin axis-damaging iron species accumulate in the circulation and within vascular cells, with potentially serious consequences for endothelial function. This review explores the mechanisms by which iron dysregulation compromises vascular endothelial cell biology across a range of disease states, including haemolytic anaemias, atherosclerosis, cerebrovascular disease, extracorporeal circulatory support, and iatrogenic iron loading. Common pathological themes emerge: depletion of nitric oxide bioavailability, oxidative stress, endothelial activation, and in chronic settings, vascular remodelling. The review subsequently focuses in depth on the pulmonary vasculature, where dysregulated iron compartmentalisation has emerged as a key contributor to the pathogenesis of pulmonary hypertension. Here, iron-driven mitochondrial dysfunction, smooth muscle cell proliferation, and iron-dependent lipid peroxidation via ferroptosis are discussed as mechanistic drivers of pulmonary vascular remodelling. The therapeutic implications of targeting iron handling in pulmonary hypertension are considered, including modulation of the hepcidin-ferroportin axis. Together, the evidence presented highlights disordered iron compartmentalisation as a unifying pathological thread across vascular disease and a compelling target for intervention.
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Journal articleAlharbi R, Keles M, Fernandez N, et al., 2026,
KLF6 activation marks an angiogenic and apoptosis resistant endothelial phenotype in pulmonary arterial hypertension
, Communications Biology, ISSN: 2399-3642 -
Journal articleBarallobre-Barreiro J, Mayr M, 2026,
Proteomic insights into bi-atrial remodelling in persistent atrial fibrillation.
, Cardiovasc Res, Vol: 122, Pages: 958-959 -
Journal articleMarchetti M, Meloni M, Anwar M, et al., 2026,
Correction: Marchetti et al. MicroRNA-24-3p Targets Notch and Other Vascular Morphogens to Regulate Post-ischemic Microvascular Responses in Limb Muscles. Int. J. Mol. Sci. 2020, 21, 1733.
, Int J Mol Sci, Vol: 27In the original publication [...].
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Journal articleLundby A, Van Eyk JE, Mayr M, et al., 2026,
Consensus statement on mass spectrometry-based proteomic analysis of cardiac tissue.
, Nat Cardiovasc Res, Vol: 5, Pages: 526-540Mass spectrometry-based cardiac proteomics provides direct molecular insight into cardiac physiology and disease. While plasma proteomics has advanced biomarker discovery, the analysis of cardiac tissue is essential for mechanistic understanding and therapeutic target identification; however, proteomic investigation of cardiac tissue faces unique challenges, including limited sample availability, regional heterogeneity, variability in collection and processing, and inconsistent reporting practices that hinder reproducibility and data integration. Here, we provide a practical framework for designing and conducting mass spectrometry-based proteomic studies of cardiac tissue and primary cardiac cells. We outline best practices and key considerations for sample handling, experimental design, data acquisition, quality control and statistical analysis. This guideline aims to support cardiac researchers in generating robust and reproducible proteomics datasets that advance our understanding of cardiac biology in both physiological and pathological contexts.
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