ArticlePLoS computational biology2026
A minimal mathematical model of red blood cell homeostasis in anemia.
Article in PLoS computational biology, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anemias are diverse and cause significant morbidity and mortality, but their mechanisms are not fully understood. To unravel this complexity requires understanding how hemoglobin and red blood cell function is regulated, and what goes wrong in each form of anemia. Anemias present puzzling imbalance between hemoglobin (Hb) and the main regulator of red blood cells - the hormone erythropoietin (EPO). In some anemias EPO is markedly elevated relative to the degree of anemia, whereas in others it is inappropriately low. This variability suggests that the feedback between oxygen delivery and erythropoietin production involves mechanisms beyond simple oxygen sensing. We developed a minimal mechanistic model of erythropoiesis composed of four coupled differential equations representing erythroid progenitors, marrow reticulocytes, circulating RBCs, and plasma EPO. Most parameters were derived from experimental measurements and correspond to physiological quantities. Data from ~1,830 adults across 36 published studies, encompassing healthy individuals and patients with major anemia types, were used to validate the model, along with blood-donor recovery cohorts. The model reproduces the near-exponential Hb-EPO relationship observed in reference populations, the characteristic trajectory of hemoglobin recovery after blood loss, and disease-specific deviations through physiologically plausible parameter changes, without ad hoc fitting. Elevated EPO in aplastic anemia emerges from reduced erythroid mass and diminished receptor-mediated clearance; chronic kidney disease is consistent with impaired EPO synthesis and marrow suppression; anemia of chronic disease arises from reduced progenitor differentiation without requiring primary EPO failure; and shortened RBC lifespan alone does not lower steady-state EPO in hemolysis. Of potential clinical significance is that steady-state erythropoietin levels provide a noninvasive indicator of bone marrow activity, with higher levels reflecting reduced erythroid mass and diminished receptor-mediated uptake.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.