The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The target gene/protein is HPX encoding hemopexin, UniProt P02790, in Homo sapiens. The literature retrieved here consistently describes HPX as an extracellular/plasma heme-binding glycoprotein that scavenges free heme and delivers it to cells (notably liver) via receptor-mediated pathways, matching the UniProt description and hemopexin-family role. (li2023doubleedgedfunctionsof pages 1-2, pierro2025trackinghemopexinintracellularly pages 23-25)
Hemopexin is described as a plasma glycoprotein (~60 kDa) and the highest-affinity heme-binding protein in plasma, functioning as a systemic heme scavenger during hemolysis. (li2023doubleedgedfunctionsof pages 1-2)
The core biochemical role of HPX is to bind free heme in extracellular fluids and limit heme-mediated oxidative/inflammatory toxicity. HPX is routinely framed as a “second-line” defense in hemolysis when upstream hemoglobin scavenging (e.g., haptoglobin-bound hemoglobin) is saturated/depleted, allowing heme to accumulate and transfer to HPX. (li2023doubleedgedfunctionsof pages 2-3, li2023doubleedgedfunctionsof pages 1-2)
Stoichiometry and physiological abundance. Reviews and mechanistic literature report circulating HPX levels on the order of ~0.4–1.5 mg/mL (or ~0.5–1.5 mg/mL), and note heme binding behavior that is 1:1 at low heme concentrations but can reach ≥2:1 (heme:HPX) at higher heme loads. (li2023doubleedgedfunctionsof pages 1-2, pierro2025trackinghemopexinintracellularly pages 23-25)
HPX is fundamentally an extracellular protein present in plasma and also reported in cerebrospinal fluid and lymph. Its heme-scavenging role is linked to systemic delivery of heme to the liver, where heme is catabolized and iron handled. (pierro2025trackinghemopexinintracellularly pages 1-2)
A canonical mechanism described in recent reviews is CD91/LRP1-mediated endocytosis of heme–HPX (often highlighted for hepatic uptake/clearance). (li2023doubleedgedfunctionsof pages 1-2, li2023doubleedgedfunctionsof pages 2-3)
More recent mechanistic cell-model work extends this view by showing HPX uptake/trafficking can involve additional receptors and pathways:
- LRP1 is reported as a high-affinity HPX-binding protein with Kd ≈ 4 nM. (pierro2025trackinghemopexinintracellularly pages 2-3)
- In human immune/liver cell models, HPX trafficked with transferrin and transferrin receptor 1 (TfR1) in Rab5-positive early endosomes, consistent with clathrin-mediated endocytosis routes used by iron transport machinery; TfR2 co-localization suggests potential contribution to liver targeting. (pierro2025trackinghemopexinintracellularly pages 1-2, pierro2025trackinghemopexinintracellularly pages 6-8)
- Importantly, heme–HPX endocytosis was observed even in LRP1−/− cells, implying uptake routes beyond LRP1 alone. (pierro2025trackinghemopexinintracellularly pages 1-2)
Once internalized, heme delivered via HPX is connected to induction of a cytoprotective program, including induction of heme oxygenase-1 (HMOX1/HO-1), ferritin induction, and other antioxidant responses. (pierro2025trackinghemopexinintracellularly pages 1-2, montecinos2019whatisnext pages 1-3)
Reviews also link heme–HPX delivery to transcriptional regulation of HO-1 via relief of Bach1 repression and to broader iron-handling systems (IRP/IRE and ferritin storage). (montecinos2019whatisnext pages 1-3)
A 2023 peer-reviewed review (“Double-edged functions of hemopexin in hematological related diseases”) compiles evidence that HPX is frequently depleted/insufficient in hemolysis-driven conditions (e.g., SCD, transfusion-induced hemolysis, sepsis), motivating HPX supplementation and related approaches, while also noting potential deleterious effects in some contexts. The review summarizes translational strategies including recombinant production, modification/enhancement, combined scavenger strategies, and gene-therapy concepts. (li2023doubleedgedfunctionsof pages 1-2, li2023doubleedgedfunctionsof pages 9-10)
The same review cites diverse disease associations of HPX levels (e.g., sepsis outcomes, malaria severity relationships, CNS hemorrhage contexts) and notes a phase 1 clinical trial mention in sickle cell anemia (NCT04285827, as cited within the review). (li2023doubleedgedfunctionsof pages 8-9)
A 2024 review on priapism in sickle cell disease emphasizes that intravascular hemolysis in SCD can reduce haptoglobin and hemopexin levels, contributing to accumulation of free hemoglobin/heme and downstream inflammatory signaling. The review frames reducing excess free heme as a therapeutic concept relevant to priapism pathophysiology. (silveira2024targetinghemein pages 2-3)
A 2024 Frontiers in Immunology primary study measured plasma heme and scavengers (including hemopexin) in large cohorts of injured patients:
- 98 burn patients and 147 trauma patients sampled at ultra-early and acute timepoints (≤1 hour and 4–72 hours post injury). (tullie2024severethermaland pages 1-2)
- The study reports that elevated plasma heme in burns/trauma coincided with reduced hemopexin and albumin (and other scavengers), consistent with a stressed heme-scavenging system. (tullie2024severethermaland pages 1-2, tullie2024severethermaland pages 15-16)
In burns, day-1 total heme was associated with both sepsis and mortality risk; notably, a 6.5 µM higher day-1 heme corresponded to increased odds of sepsis and mortality in logistic models (details in Section 5). (tullie2024severethermaland pages 10-11)
Figure evidence for these dynamics (heme over time; scavenger protein trajectories including hemopexin) is available in the study’s panels (Figures 3 and 5). (tullie2024severethermaland media 71c61103)
A 2024 Clinical Proteomics study compared plasma proteomes in descending type B dissection (n=75) versus descending thoracic aortic aneurysm (DTAA; n=62) and found that HPX was the only protein significantly different at stringent multiple-testing thresholds. (momenzadeh2024differentiationbetweendescending pages 1-2, momenzadeh2024differentiationbetweendescending pages 5-7)
The same study used machine learning and ranked HPX among top features (permutation importance) and reported held-out performance metrics (precision–recall AUC around 0.7). (momenzadeh2024differentiationbetweendescending pages 1-2, momenzadeh2024differentiationbetweendescending pages 5-7)
Across hemolytic/inflammatory diseases, HPX is often discussed as a candidate biomarker of heme-scavenging capacity and disease stage/severity. In pediatric SCD biomarker profiling (Ghana; 2021–2022), HPX was included in a multiplex panel of “heme scavengers” (HO-1, HPX, haptoglobin) and correlated with hematologic parameters; the study also describes ROC/AUC analyses to support predictive algorithms, although numeric HPX values/AUCs were not extractable from the retrieved excerpt. (lekpor2024circulatingbiomarkersassociated pages 1-2)
In vascular disease proteomics (type B dissection vs DTAA), HPX emerged as the key differentiating protein after multiple-testing correction, demonstrating its practical appearance in real-world clinical proteomics pipelines for difficult-to-separate phenotypes. (momenzadeh2024differentiationbetweendescending pages 1-2, momenzadeh2024differentiationbetweendescending pages 7-9)
Recent reviews emphasize restoration of heme scavenging as a therapeutic direction when endogenous HPX is depleted. Strategies discussed include HPX supplementation, combined Hb/heme scavenger approaches (Hp+HPX), recombinant HPX production, fusion proteins, and viral gene delivery concepts (e.g., AAV-mediated sustained expression) as preclinical-to-translational approaches. (li2023doubleedgedfunctionsof pages 9-10, li2023doubleedgedfunctionsof pages 1-2)
Mechanistic literature frames HPX not only as a heme sink but as a ligand delivery system that initiates regulated cellular responses. Heme–HPX endocytosis is linked to HO-1 induction and coordinated iron handling (ferritin induction, transferrin receptor downregulation), implying HPX participates in heme-responsive homeostatic programming rather than simple neutralization. (pierro2025trackinghemopexinintracellularly pages 1-2, montecinos2019whatisnext pages 1-3)
While CD91/LRP1 is often presented as the canonical uptake route, newer cell work suggests multiple receptors and endocytic routes (TfR1/TfR2 involvement; uptake in LRP1−/− cells), which has implications for tissue targeting, drug design (engineered HPX), and interpretation of HPX behavior in immune versus hepatic settings. (pierro2025trackinghemopexinintracellularly pages 1-2, pierro2025trackinghemopexinintracellularly pages 6-8)
The 2023 review explicitly cautions that HPX may be protective in many heme-overload contexts yet could have deleterious associations/impacts in certain settings, arguing for context-specific evaluation (e.g., timing, compartment, concurrent hemoglobin/heme loads, organ vulnerability). This is consistent with the broader theme that heme biology and scavenger systems can both buffer toxicity and modulate immune/vascular pathways. (li2023doubleedgedfunctionsof pages 9-10)
In the 2024 burns/trauma cohort study:
- Burns cohort: n=98 enrolled; sepsis assessed in n=79, with 42/79 (53%) developing sepsis. (tullie2024severethermaland pages 10-11)
- A 6.5 µM higher day-1 total heme was associated with:
- Sepsis (unadjusted): OR 1.24 (95% CI 1.05–1.46), p=0.013; adjusted (age, gender, %TBSA): OR 1.12 (0.95–1.33), p=0.172. (tullie2024severethermaland pages 10-11)
- Mortality (unadjusted): OR 1.63 (1.12–2.37), p=0.004; adjusted: OR 1.52 (1.02–2.28), p=0.021. (tullie2024severethermaland pages 10-11)
- Discrimination of survivors vs non-survivors using day-1 heme: AUROC 0.768 (95% CI 0.615–0.922) vs rBAUX AUROC 0.718. (tullie2024severethermaland pages 10-11)
Although numeric plasma hemopexin concentrations were not present in the extracted text snippets, the paper reports hemopexin trajectories and depletion after injury, and the relevant visual evidence is in panels showing hemopexin over time (Figure 5). (tullie2024severethermaland media 71c61103)
In the 2024 Clinical Proteomics study:
- Sample sizes: 75 descending type B dissection vs 62 DTAA (total 137). (momenzadeh2024differentiationbetweendescending pages 1-2, momenzadeh2024differentiationbetweendescending pages 5-7)
- HPX was the only significantly different protein after correction, with Log2FC = −0.25 and B-H adjusted p = 0.0081 (Table 2). (momenzadeh2024differentiationbetweendescending pages 7-9)
- ML performance reported includes a held-out test-set precision–recall AUC ≈ 0.7; additional metrics in extracted text include accuracy 0.74 and F1-score 0.67 for the optimized SVC model. (momenzadeh2024differentiationbetweendescending pages 1-2, momenzadeh2024differentiationbetweendescending pages 5-7)
Mechanistic literature reports LRP1 binding Kd ≈ 4 nM for HPX, supporting high-affinity receptor-mediated uptake. (pierro2025trackinghemopexinintracellularly pages 2-3)
Reported plasma concentrations of HPX are ~0.4–1.5 mg/mL (≈15.3 µM average in one synthesis), providing a scale for heme-buffering capacity. (pierro2025trackinghemopexinintracellularly pages 23-25)
The following table consolidates HPX functional annotation, pathway placement, and key recent quantitative findings.
| Category | Key points | Quantitative data (if any) | Key sources (with citation IDs) |
|---|---|---|---|
| Protein type / localization | Human HPX (UniProt P02790) corresponds to hemopexin, a secreted/plasma glycoprotein and major extracellular heme scavenger. It is primarily produced by liver and is also reported in nervous tissue, skeletal muscle, retina, and kidney; HPX is present in plasma and also detected in CSF and lymph. | ~60 kDa; plasma concentration reported 0.4–1.5 mg/mL or 0.5–1.5 mg/mL; ≈15.3 µM average in one recent study/review synthesis. | (li2023doubleedgedfunctionsof pages 1-2, pierro2025trackinghemopexinintracellularly pages 23-25) |
| Primary ligand / substrate | Primary ligand is free heme (including heme released during hemolysis and heme transferred from other plasma carriers). HPX is described as the highest-affinity heme-binding protein in plasma and a second-line defense after haptoglobin depletion. | Heme–HPX forms a 1:1 complex; each mL plasma can bind 6.3 mg heme according to a 2023 review summary. | (pierro2025trackinghemopexinintracellularly pages 2-3, li2023doubleedgedfunctionsof pages 1-2, li2023doubleedgedfunctionsof pages 2-3, li2023doubleedgedfunctionsof pages 8-9) |
| Binding stoichiometry / concentration ranges | HPX binds heme tightly at physiologic pH and releases it in acidic endosomal compartments. At low heme, binding is 1:1; at higher heme loads, reports indicate ≥2:1 (heme:HPX) binding behavior. | Stoichiometry: 1:1 at low heme; ≥2:1 at higher heme. Plasma HPX: 0.4–1.5 mg/mL / 0.5–1.5 mg/mL; one review cites average plasma HPX 770 mg/mL but this value is likely inconsistent with the broader literature and should be treated cautiously. | (li2023doubleedgedfunctionsof pages 1-2, pierro2025trackinghemopexinintracellularly pages 23-25, li2023doubleedgedfunctionsof pages 8-9) |
| Receptors / uptake pathways | Canonical pathway is CD91/LRP1-mediated uptake of heme–HPX in liver/macrophages. Recent cell work indicates uptake is not exclusively LRP1-dependent: HPX traffics with transferrin receptor 1 (TfR1) in Rab5-positive early endosomes, and TfR2 may contribute to hepatic targeting; uptake also occurs in LRP1−/− cells, implying alternative receptors. | LRP1 Kd ≈ 4 nM for HPX binding; LRP1 described as a high-affinity HPX-binding protein. | (pierro2025trackinghemopexinintracellularly pages 2-3, pierro2025trackinghemopexinintracellularly pages 1-2, li2023doubleedgedfunctionsof pages 2-3, pierro2025trackinghemopexinintracellularly pages 6-8) |
| Downstream intracellular fate / pathway | After endocytosis, heme is delivered intracellularly and induces a cytoprotective program: HMOX1/HO-1 induction, ferritin induction, transferrin receptor downregulation, metallothionein induction, and coupling to iron storage/export pathways. Heme degradation yields bilirubin, CO, and iron; iron is stored in ferritin or exported via ferroportin. Apo-HPX may recycle in some settings. | Free heme uptake can occur at ~5-fold higher molar rate than heme–HPX uptake; intracellular heme levels of 3 µM (~1 million heme molecules in mitochondrial volume) were reported in hepatocyte-focused review literature. | (pierro2025trackinghemopexinintracellularly pages 1-2, montecinos2019whatisnext pages 1-3, li2023doubleedgedfunctionsof pages 2-3) |
| Key disease contexts: SCD / hemolysis | HPX is depleted in hemolytic states including sickle cell disease (SCD), where low HPX is linked to heme overload, vaso-occlusion, AKI risk, and priapism-related pathophysiology. Reviews note lower HPX in SCD vaso-occlusive crisis versus steady state and increases with hydroxycarbamide/hydroxyurea as hemolysis declines. | No exact cohort HPX concentration from the gathered 2024 SCD biomarker study excerpt; pediatric SCD study included 377 children aged 3–8 years. | (li2023doubleedgedfunctionsof pages 8-9, silveira2024targetinghemein pages 2-3, li2023doubleedgedfunctionsof pages 2-3, lekpor2024circulatingbiomarkersassociated pages 1-2) |
| Key disease contexts: sepsis / trauma / burn | In inflammatory/hemolytic injury states, HPX is often insufficient relative to heme burden. Major trauma and burns show elevated plasma heme with reduced hemopexin and albumin, supporting failure of the scavenging system and motivating HPX restoration concepts. | Trauma cohort: 147 patients (mean age 42, mean ISS 25). Burn cohort: 98 patients (mean age 47, mean TBSA 35%). Heme correlated with burn severity: %TBSA r=0.456, % full-thickness TBSA r=0.466, Baux r=0.350, revised Baux r=0.390; trauma heme vs time r=-0.452. | (tullie2024severethermaland pages 1-2, tullie2024severethermaland pages 15-16, tullie2024severethermaland pages 6-7) |
| Key disease contexts: CNS hemorrhage | HPX is implicated in CNS blood-breakdown product handling. Review evidence indicates CSF HPX can associate with outcomes after intracranial hemorrhage, though direction differs by condition: better outcomes in some ICH contexts but worse in SAH in others. HPX is also discussed as protective in intracerebral hemorrhage models. | No consistent single quantitative effect size for HPX across CNS hemorrhage contexts in the gathered evidence. | (montecinos2019whatisnext pages 1-3, li2023doubleedgedfunctionsof pages 8-9) |
| Therapeutic / clinical translation | Translational strategies include HPX supplementation during endogenous depletion, combined Hp+HPX approaches, recombinant rhHPX production, hemopexin–haptoglobin fusion proteins, and AAV-based HPX gene therapy concepts. A phase 1 study in sickle cell anemia is mentioned in review literature. | Clinical trial mention: NCT04285827 (phase 1 HPX in sickle cell anemia, as cited in the 2023 review). AAV-mediated expression reported for 58 days with survival after experimental heme challenge in preclinical work summarized by the review. | (li2023doubleedgedfunctionsof pages 8-9, li2023doubleedgedfunctionsof pages 9-10, li2023doubleedgedfunctionsof pages 1-2) |
| Quantitative findings from 2024 trauma/burn study | Burn/trauma study provides the clearest recent human quantitative evidence linking excess heme and depleted scavenging proteins. Hemopexin was significantly reduced on day 1/day 3 post-injury, though exact HPX concentrations were not reported in the extracted evidence. | Burns: day 3 heme 17.03 ± 0.92 µM vs healthy controls 17.59 ± 1.47 µM (ns). In burns, 6.5 µM higher day-1 heme associated with sepsis odds OR 1.24 (95% CI 1.05–1.46, p=0.013), adjusted OR 1.12 (0.95–1.33, p=0.172); mortality odds OR 1.63 (1.12–2.37, p=0.004), adjusted OR 1.52 (1.02–2.28, p=0.021). AUROC for mortality using day-1 heme: 0.768 (95% CI 0.615–0.922) vs rBAUX 0.718. Sepsis assessed in 79 burn patients; 42 developed sepsis (53%). | (tullie2024severethermaland pages 1-2, tullie2024severethermaland pages 15-16, tullie2024severethermaland pages 10-11, tullie2024severethermaland pages 6-7, tullie2024severethermaland media 71c61103) |
Table: This table summarizes the functional annotation of human HPX/hemopexin, emphasizing ligand binding, uptake pathways, intracellular fate, disease relevance, and recent translational findings. It is designed as a compact evidence map for narrative reporting and citation-supported interpretation.
References
(li2023doubleedgedfunctionsof pages 1-2): Yijin Li, Renyu Chen, Chaofan Wang, Jun Deng, and Shanshan Luo. Double-edged functions of hemopexin in hematological related diseases: from basic mechanisms to clinical application. Frontiers in Immunology, Nov 2023. URL: https://doi.org/10.3389/fimmu.2023.1274333, doi:10.3389/fimmu.2023.1274333. This article has 11 citations and is from a peer-reviewed journal.
(pierro2025trackinghemopexinintracellularly pages 23-25): E. Pierro, T. L. Duarte, Hans Bäumler, B. Rose, D. Moore, J. Eskew, R. Vanacore, S. Hartson, Dennis W. Province, D. Skaff, and Ann Smith. Tracking hemopexin intracellularly and defining hemopexin protein “interactomes” in human immune and liver cell models. Frontiers in Physiology, Nov 2025. URL: https://doi.org/10.3389/fphys.2025.1613917, doi:10.3389/fphys.2025.1613917. This article has 0 citations.
(li2023doubleedgedfunctionsof pages 2-3): Yijin Li, Renyu Chen, Chaofan Wang, Jun Deng, and Shanshan Luo. Double-edged functions of hemopexin in hematological related diseases: from basic mechanisms to clinical application. Frontiers in Immunology, Nov 2023. URL: https://doi.org/10.3389/fimmu.2023.1274333, doi:10.3389/fimmu.2023.1274333. This article has 11 citations and is from a peer-reviewed journal.
(pierro2025trackinghemopexinintracellularly pages 1-2): E. Pierro, T. L. Duarte, Hans Bäumler, B. Rose, D. Moore, J. Eskew, R. Vanacore, S. Hartson, Dennis W. Province, D. Skaff, and Ann Smith. Tracking hemopexin intracellularly and defining hemopexin protein “interactomes” in human immune and liver cell models. Frontiers in Physiology, Nov 2025. URL: https://doi.org/10.3389/fphys.2025.1613917, doi:10.3389/fphys.2025.1613917. This article has 0 citations.
(pierro2025trackinghemopexinintracellularly pages 2-3): E. Pierro, T. L. Duarte, Hans Bäumler, B. Rose, D. Moore, J. Eskew, R. Vanacore, S. Hartson, Dennis W. Province, D. Skaff, and Ann Smith. Tracking hemopexin intracellularly and defining hemopexin protein “interactomes” in human immune and liver cell models. Frontiers in Physiology, Nov 2025. URL: https://doi.org/10.3389/fphys.2025.1613917, doi:10.3389/fphys.2025.1613917. This article has 0 citations.
(pierro2025trackinghemopexinintracellularly pages 6-8): E. Pierro, T. L. Duarte, Hans Bäumler, B. Rose, D. Moore, J. Eskew, R. Vanacore, S. Hartson, Dennis W. Province, D. Skaff, and Ann Smith. Tracking hemopexin intracellularly and defining hemopexin protein “interactomes” in human immune and liver cell models. Frontiers in Physiology, Nov 2025. URL: https://doi.org/10.3389/fphys.2025.1613917, doi:10.3389/fphys.2025.1613917. This article has 0 citations.
(montecinos2019whatisnext pages 1-3): Luis Montecinos, Jeffrey D. Eskew, and Ann Smith. What is next in this “age” of heme-driven pathology and protection by hemopexin? an update and links with iron †. Pharmaceuticals, 12:144, Sep 2019. URL: https://doi.org/10.3390/ph12040144, doi:10.3390/ph12040144. This article has 33 citations.
(li2023doubleedgedfunctionsof pages 9-10): Yijin Li, Renyu Chen, Chaofan Wang, Jun Deng, and Shanshan Luo. Double-edged functions of hemopexin in hematological related diseases: from basic mechanisms to clinical application. Frontiers in Immunology, Nov 2023. URL: https://doi.org/10.3389/fimmu.2023.1274333, doi:10.3389/fimmu.2023.1274333. This article has 11 citations and is from a peer-reviewed journal.
(li2023doubleedgedfunctionsof pages 8-9): Yijin Li, Renyu Chen, Chaofan Wang, Jun Deng, and Shanshan Luo. Double-edged functions of hemopexin in hematological related diseases: from basic mechanisms to clinical application. Frontiers in Immunology, Nov 2023. URL: https://doi.org/10.3389/fimmu.2023.1274333, doi:10.3389/fimmu.2023.1274333. This article has 11 citations and is from a peer-reviewed journal.
(silveira2024targetinghemein pages 2-3): Tammyris Helena Rebecchi Silveira, Fabiano Beraldi Calmasini, Mariana Gonçalves de Oliveira, Fernando Ferreira Costa, and Fábio Henrique Silva. Targeting heme in sickle cell disease: new perspectives on priapism treatment. Frontiers in Physiology, Jul 2024. URL: https://doi.org/10.3389/fphys.2024.1435220, doi:10.3389/fphys.2024.1435220. This article has 9 citations.
(tullie2024severethermaland pages 1-2): Sebastian Tullie, Thomas Nicholson, Jonathan R. B. Bishop, Kirsty C. McGee, Ali Asiri, Jack Sullivan, Yung-Yi Chen, Amanda V. Sardeli, Antonio Belli, Paul Harrison, Naiem S. Moiemen, Janet M. Lord, and Jon Hazeldine. Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1416820, doi:10.3389/fimmu.2024.1416820. This article has 15 citations and is from a peer-reviewed journal.
(tullie2024severethermaland pages 15-16): Sebastian Tullie, Thomas Nicholson, Jonathan R. B. Bishop, Kirsty C. McGee, Ali Asiri, Jack Sullivan, Yung-Yi Chen, Amanda V. Sardeli, Antonio Belli, Paul Harrison, Naiem S. Moiemen, Janet M. Lord, and Jon Hazeldine. Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1416820, doi:10.3389/fimmu.2024.1416820. This article has 15 citations and is from a peer-reviewed journal.
(tullie2024severethermaland pages 10-11): Sebastian Tullie, Thomas Nicholson, Jonathan R. B. Bishop, Kirsty C. McGee, Ali Asiri, Jack Sullivan, Yung-Yi Chen, Amanda V. Sardeli, Antonio Belli, Paul Harrison, Naiem S. Moiemen, Janet M. Lord, and Jon Hazeldine. Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1416820, doi:10.3389/fimmu.2024.1416820. This article has 15 citations and is from a peer-reviewed journal.
(tullie2024severethermaland media 71c61103): Sebastian Tullie, Thomas Nicholson, Jonathan R. B. Bishop, Kirsty C. McGee, Ali Asiri, Jack Sullivan, Yung-Yi Chen, Amanda V. Sardeli, Antonio Belli, Paul Harrison, Naiem S. Moiemen, Janet M. Lord, and Jon Hazeldine. Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1416820, doi:10.3389/fimmu.2024.1416820. This article has 15 citations and is from a peer-reviewed journal.
(momenzadeh2024differentiationbetweendescending pages 1-2): Amanda Momenzadeh, Simion Kreimer, Dongchuan Guo, Matthew Ayres, Daniel Berman, Kuang-Yuh Chyu, Prediman K. Shah, Dianna Milewicz, Ali Azizzadeh, Jesse G. Meyer, and Sarah Parker. Differentiation between descending thoracic aortic diseases using machine learning and plasma proteomic signatures. Clinical Proteomics, Jun 2024. URL: https://doi.org/10.1186/s12014-024-09487-4, doi:10.1186/s12014-024-09487-4. This article has 2 citations and is from a peer-reviewed journal.
(momenzadeh2024differentiationbetweendescending pages 5-7): Amanda Momenzadeh, Simion Kreimer, Dongchuan Guo, Matthew Ayres, Daniel Berman, Kuang-Yuh Chyu, Prediman K. Shah, Dianna Milewicz, Ali Azizzadeh, Jesse G. Meyer, and Sarah Parker. Differentiation between descending thoracic aortic diseases using machine learning and plasma proteomic signatures. Clinical Proteomics, Jun 2024. URL: https://doi.org/10.1186/s12014-024-09487-4, doi:10.1186/s12014-024-09487-4. This article has 2 citations and is from a peer-reviewed journal.
(lekpor2024circulatingbiomarkersassociated pages 1-2): Cecilia Elorm Lekpor, Felix Abekah Botchway, Adel Driss, Alaijah Bashi, Afua D. Abrahams, Kwadwo Asamoah Kusi, Godfred Futagbi, Ernest Alema-Mensah, William Agbozo, Wesley Solomon, Adriana Harbuzariu, Andrew A. Adjei, and Jonathan K. Stiles. Circulating biomarkers associated with pediatric sickle cell disease. Frontiers in Molecular Biosciences, Dec 2024. URL: https://doi.org/10.3389/fmolb.2024.1481441, doi:10.3389/fmolb.2024.1481441. This article has 5 citations.
(momenzadeh2024differentiationbetweendescending pages 7-9): Amanda Momenzadeh, Simion Kreimer, Dongchuan Guo, Matthew Ayres, Daniel Berman, Kuang-Yuh Chyu, Prediman K. Shah, Dianna Milewicz, Ali Azizzadeh, Jesse G. Meyer, and Sarah Parker. Differentiation between descending thoracic aortic diseases using machine learning and plasma proteomic signatures. Clinical Proteomics, Jun 2024. URL: https://doi.org/10.1186/s12014-024-09487-4, doi:10.1186/s12014-024-09487-4. This article has 2 citations and is from a peer-reviewed journal.
(tullie2024severethermaland pages 6-7): Sebastian Tullie, Thomas Nicholson, Jonathan R. B. Bishop, Kirsty C. McGee, Ali Asiri, Jack Sullivan, Yung-Yi Chen, Amanda V. Sardeli, Antonio Belli, Paul Harrison, Naiem S. Moiemen, Janet M. Lord, and Jon Hazeldine. Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1416820, doi:10.3389/fimmu.2024.1416820. This article has 15 citations and is from a peer-reviewed journal.