Resolvins may drive fibrosis in aged cells rather than resolve it
A worn-out FPR2 receptor does not merely respond weakly to resolvins. It switches them to a β-arrestin-biased output that reinforces TGF-β1 production, which would make supplementing aged tissue with these pro-resolution molecules actively harmful rather than simply ineffective.
Omega Point 1.0
Stage of verification
- Hypothesis published2026-09-14
- Indirect evidenceAssessed at 4 of 10
- Direct testAwaited
Map of the hypothesis
Hover over an icon or tap it to see its name.
Where in the body
Biological function
Lens
Kind of knowledge gap
A double ring marks the main placement where a group contains several values.
Target map
Every target of every published hypothesis, each with the actions a hypothesis can propose on it. The targets and the actions of this hypothesis are drawn solid.
Receptor or channel
FPR2/ALX receptor
A receptor whose signaling output can depend on its phosphorylation and desensitization state
Where this hypothesis actsAged human macrophages with desensitized receptors and documented low FPR2 surface density
Hypotheses on this target 1
Lower level
Higher level
Blockade
Agonism1
Desensitisation
Function restoration
Function preservation
What is proposed
Agonism
Stimulate the receptor with resolvin D1
With whatSmall molecule
HowTreat aged human macrophages with resolvin D1 and measure TGF-β1 secretion by ELISA
Possible result
Possible increase in TGF-β1 secretion through β-arrestin-biased signaling
From the recordIn aged human macrophages with documented low FPR2 surface density, resolvin D1 treatment will increase TGF-β1 secretion above untreated controls
Regulatory protein
β-arrestin-2
A protein implicated in β-arrestin-biased receptor signaling
Where this hypothesis actsAged human macrophages with low FPR2 surface density during resolvin D1 treatment
Hypotheses on this target 1
Inhibition
Activation- Lower level1
- Higher level
Protection from degradation- Function restoration
- Function preservation
What is proposed
Lower level
Suppress β-arrestin-2 using siRNA
With whatRNA interference or antisense
HowUse β-arrestin-2 siRNA during resolvin D1 treatment and measure TGF-β1 secretion
Possible result
Expected blockade of the resolvin D1-induced increase in TGF-β1 secretion
From the recordthis increase will be blocked by β-arrestin-2 siRNA but not by pertussis toxin (Gαi inhibitor)
All targets of the lab
Every target read from the published hypotheses, each kind around its pictogram. A larger mark means more hypotheses act on that target. Point at a mark and the actions proposed on it branch out of it.
Solid and named: the targets of this hypothesis
Explore in depth
The logic
The train of thought that ends in this hypothesis. Each stage is the reason the next exists. The master question narrows to a goal, the goal to an unknown nobody has closed, the unknown to the hypothesis proposed here. Every step below says what it rests on and what carries it.
Restoring the surroundings that support stem cells may require understanding when signals that normally end inflammation could instead encourage scarring. The unexpected move is a proposed reversal: an aged cell would respond to the same molecule with a different kind of message, rather than simply responding less strongly. This is a hypothesis generated by the pipeline, not a measured reversal.
- Age-associated desensitization is proposed to alter formyl peptide receptor 2, also called ALX, a cell-surface receiver for resolvin D1.
- Resolvin D1 acting on that altered receptor is proposed to switch output from an inflammation-limiting route using inhibitory G protein alpha i, an internal signal relay, to a scarring-promoting route favoring beta-arrestin, a protein that regulates receptors and carries signals.
- The beta-arrestin route is proposed to activate extracellular signal-regulated kinases 1 and 2, enzymes that relay signals, and their interaction with SMAD3, a protein that carries signals to gene-control machinery.
- That interaction is proposed to cooperate with interferon regulatory factor 4 and signal transducer and activator of transcription 6, proteins that regulate gene activity, at an enhancer, a DNA region controlling output of the gene for transforming growth factor beta 1.
- Increased gene activity is proposed to increase release of transforming growth factor beta 1 from aged macrophages.
- The increased signal is proposed to favor fibrosis, the buildup of scar-like tissue, rather than resolution of the niche's damaging conditions.
A worn doorbell might simply become quieter; this proposal instead imagines its button becoming connected to an alarm. The same press would then trigger a different response.
Where the picture breaks: Cellular signaling is not a fixed wire connecting one button to one output. Measuring fewer receptors on a cell does not establish that the remaining receptors have changed their signaling route.
- Master questionstep 01 of 04
Rejuvenating the stem cell niche—the local cells, materials and signals that support stem cells—is the overall goal.
Rests on: The goal treats the condition of stem cells' surroundings as a target for rejuvenation.
Stated in the chain - Goal pillarstep 02 of 04
Weakening a self-reinforcing loop between tissue mechanics, meaning physical properties and forces, and inflammation is selected as a route toward rejuvenation.
Rests on: The master question identifies the surroundings of stem cells as the target, but does not identify this particular loop as a cause of their decline.
AssumptionThe pillar assumes that mechanical conditions and inflammation reinforce one another in the relevant niche and that weakening this loop would help rejuvenate it.
- Gap questionstep 03 of 04
Specialized pro-resolving mediators, molecules that help bring inflammation to an end, might increase or decrease a scarring-related signal when they push human macrophages, immune cells that clear material and coordinate tissue responses, toward an M2 state, a repair-associated pattern of activity. The signal is transforming growth factor beta 1, a protein involved in tissue repair and scarring. The question assumes humans lack a particular chemical marking of DNA proposed to separate inflammation resolution from scarring in Acomys, the spiny mouse.
Rests on: The pillar supplies a reason to examine connections between inflammation and tissue changes, but does not establish the proposed species difference or this particular cellular route.
AssumptionThe absence in humans of the stated spiny-mouse DNA-marking mechanism is taken as given. Neither the preceding stage nor the supplied source descriptions establishes that premise.
- Hypothesisstep 04 of 04
Resolvin D1 is proposed to promote scarring in aged macrophages because a desensitized receptor, a cell-surface receiver with an altered response after stimulation, changes which internal signaling route it uses. The proposed change would amplify production of transforming growth factor beta 1 rather than merely weaken inflammation resolution.
Rests on: The gap question identifies the uncertain direction of the scarring-related signal. The endpoint then invokes receptor desensitization attributed to an internal record whose contents are not supplied and adds a proposed switch in signaling.
LeapThe missing bridge is a basis for turning reduced receptor responsiveness into an opposite, scarring-promoting output. The preceding stage and screened sources do not supply that bridge or the downstream sequence; the issue is the missing connection, not the fact that the endpoint is an untested proposal.
What is carried, and what is not. One screened source speaks directly to a component of the proposed mechanism: the 2012 American Journal of Pathology study reports resolvin-related activation of receptors in engineered beta-arrestin assays, but does not establish an age-dependent switch or scarring-promoting output. No supplied source establishes the sequence end to end; the 2021 Cardiovascular Research study instead reports reduced scarring in the right upper heart chamber in rats with experimental right-heart disease, which does not settle the proposed effect in aged human macrophages.
Where the reasoning is carried by something unstated · 3
- Goal pillar. The pillar assumes that mechanical conditions and inflammation reinforce one another in the relevant niche and that weakening this loop would help rejuvenate it.
- Gap question. The absence in humans of the stated spiny-mouse DNA-marking mechanism is taken as given. Neither the preceding stage nor the supplied source descriptions establishes that premise.
- Hypothesis. The missing bridge is a basis for turning reduced receptor responsiveness into an opposite, scarring-promoting output. The preceding stage and screened sources do not supply that bridge or the downstream sequence; the issue is the missing connection, not the fact that the endpoint is an untested proposal. Establish the missing link before relying on this step.
How a result here could mislead · 3
- Low receptor abundance at the cell surface could be read as proof of the proposed altered receptor state. The specified flow cytometry, a method for measuring features of individual cells, measures surface abundance; it does not by itself establish desensitization or phosphorylation, the attachment of phosphate groups that the hypothesis makes central. What closes it: Surface abundance must be distinguished from receptor responsiveness and phosphorylation state. A claim of reversed output also requires a comparison with cells in the proposed responsive state, not only treated and untreated cells with low receptor abundance.
- A rise in transforming growth factor beta 1 that disappears after reducing beta-arrestin-2 could be credited specifically to the proposed receptor switch, although dependence on that signaling protein alone does not identify the receptor or establish the full downstream route. What closes it: The test must establish dependence on formyl peptide receptor 2 and verify both interventions: that small interfering RNA, a method for reducing production of a selected protein, reduces beta-arrestin-2, and that pertussis toxin blocks the intended inhibitory G protein route. The supplied design does not specify these verification controls.
- More transforming growth factor beta 1 in the assay could be treated as evidence of more scarring in a tissue niche. The rival explanations instead allow its production to depend on the stiffness of the culture surface, or its action on neighboring cells to be blocked despite increased release. What closes it: Culture stiffness must be controlled, and the enzyme-linked immunosorbent assay, an antibody-based protein measurement, must specify whether it measures total or active transforming growth factor beta 1. Establishing the proposed tissue consequence additionally requires measuring responses in fibroblasts, cells that produce surrounding structural material; those measurements are not specified.
What would make this wrong. Under verified conditions of the proposed altered receptor state, resolvin D1 failing to increase transforming growth factor beta 1 above untreated controls would contradict the endpoint's defining prediction. An increase that persists despite verified reduction of beta-arrestin-2, or that requires the inhibitory G protein route instead, would contradict the proposed signaling switch. The supplied material sets no dose, treatment duration or decision threshold for these judgments.
What it would change. If the proposed reversal held, efforts to rejuvenate stem-cell surroundings by promoting inflammation resolution would have to account for receptor state: supplying more of the same signal could increase a scarring-related output in some aged cells. That would make altered signal routing a possible obstacle alongside insufficient signal strength. Even a positive result in isolated human macrophages would leave actual tissue scarring, stem-cell recovery and lasting niche rejuvenation unestablished.
Sources read · 4
Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs. · The American journal of pathology · 2012
“In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing β-arrestin systems using luminescence and electric cell–substrate impedance sensing.”
Does not settle: This source text does not establish receptor desensitization or phosphorylation-state-dependent switching of RvD1/FPR2 signaling to a pro-fibrotic β-arrestin output. It does not report ERK1/2–SMAD3 crosstalk, IRF4/STAT6 or TGFB1-enhancer activity, fibrosis endpoints, aged macrophages, or opposite RvD1 outputs in human cells.
Peripheral Interaction of Resolvin D1 and E1 with Opioid Receptor Antagonists for Antinociception in Inflammatory Pain in Rats. · Frontiers in molecular neuroscience · 2017
“Pathways include a phosphorylation cascade inhibiting the adenylate cyclase or ERK (Park et al., ; Serhan, ; Lim et al., ) or β-arrestin coupled to resolvin receptors (Krishnamoorthy et al., ).”
Does not settle: This source does not establish FPR2/ALX desensitization, a switch to β-arrestin-biased signaling, ERK1/2–SMAD3 crosstalk, TGFB1 enhancer effects, fibrosis, aged macrophages, or human receptor-phosphorylation-dependent opposite outputs.
Resolvin D1 binds human phagocytes with evidence for proresolving receptors. · Proceedings of the National Academy of Sciences of the United States of America · 2010
“These results indicate that RvD1 specifically interacts with both ALX and GPR32 on phagocytes and suggest that each plays a role in resolving acute inflammation.”
Does not settle: This source does not test aged or desensitized macrophages, receptor phosphorylation states, a switch to beta-arrestin-biased signaling, ERK1/2–SMAD3 crosstalk, IRF4/STAT6 or TGFB1 enhancer activity, fibrosis endpoints, or whether RvD1 produces pro-fibrotic effects.
The inflammation-resolution promoting molecule resolvin-D1 prevents atrial proarrhythmic remodelling in experimental right heart disease. · Cardiovascular research · 2021
“RvD1 strongly attenuated RA fibrosis but had no effect on RA dilation.”
Does not settle: This rat right-heart-disease study does not establish effects in aged human macrophages, FPR2/ALX phosphorylation or desensitization, β-arrestin bias, ERK1/2–SMAD3 crosstalk, or TGFB1-enhancer regulation.
The gap this hypothesis explains
Two established results predict opposite outcomes, and both cannot be right.
Do resolution signals make human repair macrophages release more of the scarring protein, or less?
Original wording · exactly as the pipeline generated it
Does SPM-driven M2 polarization in human niche macrophages increase or decrease TGF-β1 secretion, given that the Acomys IRF4-half-site CpG methylation decoupling pro-resolution from fibrosis is absent in humans?
What this question is asking
The question asks whether signals that help inflammation end also increase or decrease a protein that can promote scarring. Specifically, it asks whether specialized pro-resolving mediators (SPMs) push macrophages in the human stem cell niche toward an M2 repair-associated state and change their release of transforming growth factor beta 1 (TGF-β1), compared with otherwise comparable cells without that treatment. Its premise is that African spiny mice have a chemical mark at an interferon regulatory factor 4 (IRF4) half-site that separates inflammation resolution from scarring, and that humans lack this arrangement; the supplied sources do not establish that premise. The desired outcome is clearance of debris associated with senescent cells without activating scar-producing fibroblasts.
- Macrophage
- An immune cell that takes up cells and debris and releases signals that affect surrounding tissue. Its cleanup and signaling activities are the two functions being compared here.
- Inflammation resolution and specialized pro-resolving mediators (SPMs)
- Resolution is the process through which inflammation subsides. Specialized pro-resolving mediators are a class of signaling molecules associated with that process; the question asks whether their effects on cleanup also change a scar-promoting signal.
- M1, M2, polarization, and differentiation
- M1 and M2 are conventional labels for broadly inflammation-associated and repair-associated macrophage states. Polarization and differentiation describe shifts in cell characteristics; these labels summarize varied states rather than two fixed types, and M2 does not itself mean scar-free repair.
- Stem cell niche
- The local cells, signals, and physical surroundings that support stem cells, which can produce replacement cells. The question concerns macrophages in that environment, but the supplied input does not identify a particular human tissue niche.
- Transforming growth factor beta 1 (TGF-β1) and TGFB1
- TGF-β1 is a signaling protein described here in both inflammation-reducing and scar-promoting roles. TGFB1 names the gene encoding it; a change in gene expression does not by itself establish a change in protein release.
- Gene expression and protein secretion
- Gene expression is the use of genetic instructions to produce a cell's products. Secretion is release of a substance from the cell; the question asks about secretion, while S2 and S4 report expression of the gene encoding the protein.
- Fibroblast, fibroblast activation, fibrosis, and collagen
- Fibroblasts are cells that produce material supporting tissue, including the structural protein collagen. Activation can increase this activity, while fibrosis means excessive buildup of scar-like material; collagen uptake is removal into cells, not a direct measurement of scar formation.
- Senescent cells and aged red blood cells
- In the proposed niche problem, senescent cells are cells in a lasting state of no longer dividing. S7 concerns aged red blood cells, which carry oxygen; the supplied material does not establish that clearing them represents clearance of the senescent cells intended by the gap.
- Efferocytosis
- The process by which cells such as macrophages take up and clear dying cells. The sources use it for cleanup outcomes, which must be distinguished from measurements of released signaling proteins.
- Acomys
- The genus of African spiny mice named in the question. The proposed mechanism in these animals and its claimed absence in humans are premises under audit, not findings established by the supplied sources.
- Interferon regulatory factor 4 (IRF4) and half-site
- IRF4 is a protein that regulates gene activity by participating in binding to genetic material. A half-site is part of a larger binding pattern; the input proposes a mechanism involving such a site but supplies no establishing evidence.
- CpG methylation
- CpG denotes a cytosine followed by a guanine in deoxyribonucleic acid, the material carrying genetic instructions; the letter p represents the connecting phosphate. Methylation is addition of a chemical mark at such a site, proposed here to alter the relationship between inflammation resolution and scarring.
- Co-binding
- Binding involving more than one participant at a site or target. The gap description uses this term for IRF4 and TGF-β1 without specifying the participants' roles or binding target, so its precise meaning is not established here.
- Human monocyte-derived macrophages
- Macrophages developed from human monocytes, a type of blood immune cell. Findings in these cells do not by themselves establish the same response in macrophages within a stem cell niche.
- Corneal fibroblasts, ultraviolet B, and physical separation
- Corneal fibroblasts are support-producing cells from the eye's clear front surface. S2 uses ultraviolet B light to injure these cells and a compartment-separated laboratory setup involving macrophages; this is a different setting from the human niche specified in the question.
- Itaconate
- A molecule produced through cellular chemical processing. S4 links its late production to resolution-associated macrophage changes, but does not test the specialized pro-resolving mediator intervention asked about.
- Matrix metalloproteinase 8
- An enzyme involved in breaking down material surrounding cells. S4 reports its reduction alongside other changes, without establishing the requested TGF-β1 secretion outcome.
- 17R-resolvin D2
- The particular resolution-promoting signaling molecule studied in S7. Its reported effects on macrophage state and cell clearance provide nearby evidence, but not the requested measurement of TGF-β1 release.
- Glutamine metabolism
- The chemical processing of glutamine, a molecule cells use as a nutrient and building material. S5 connects that processing to M2 polarization without establishing the secretion response in the question.
Acomys IRF4-half-site CpG methylation decouples pro-resolution from fibrosis, and this decoupling mechanism is absent in humans.
The assumption concerns African spiny mice, a proposed short genetic binding site for a protein that regulates gene activity, and a chemical mark at that site. It claims that the mark lets inflammation subside without triggering scarring in these mice, while humans lack that separation. If established, this would supply a species-specific reason to question whether repair signals have the same scarring consequences in humans.
The supplied search results do not return work establishing either the proposed mouse mechanism or its absence in humans. S2 and S4 report changes in gene expression in other settings, S7 reports repair-associated and clearance effects of a resolution signal, and S5 and S9 concern other aspects of macrophage activity. None establishes the asserted species difference; this bounded set of sources does not show that the premise is false.S2S4S5S7S9
The same question asked without the part nothing read establishes:
- Does treatment with specialized pro-resolving mediators increase or decrease TGF-β1 release as macrophages in the human stem cell niche adopt an M2 repair-associated state?
- In macrophages in the human stem cell niche, does treatment with specialized pro-resolving mediators support debris clearance without increasing TGF-β1 release or fibroblast activation?
- TGF-β1 release increases Under the question's proposed mechanism, a treatment that promotes debris clearance would also increase a signal capable of activating fibroblasts. Clearance and scar-promoting activity could therefore rise together, so the repair-associated cell state would not by itself establish the desired separation.
- TGF-β1 release decreases If debris clearance also improved, the treatment would combine greater removal of unwanted material with less release of this scar-promoting signal. That would fit the requested separation at the level of these two measurements, but would not by itself establish reduced tissue scarring.
- No consistent direction If release remained unchanged or differed across conditions, the M2 label would not identify a consistent change in this signal. Any improvement in clearance would then leave the proposed effect on fibroblast activation unresolved.
The proposed chain starts with a signal changing the activity of tissue-cleaning immune cells. Those cells would need to remove debris while avoiding release of enough scar-promoting signals to activate fibroblasts. If the same treatment increased TGF-β1 release, interpreting a repair-associated cell state as evidence of scar-free repair could be mistaken. If it decreased release, assuming that repair-associated activity necessarily increases this scarring signal could also be mistaken. Neither direction alone would establish restoration of the environment that supports stem cells.
Two S-nodes predict opposite TGF-β1 outcomes from the same SPM intervention in human macrophages.
Macrophage polarization state that clears senescent debris without TGF-β1-driven fibroblast activation.
No human niche macrophage data on IRF4-TGF-β1 co-binding status during SPM-driven polarization; intervention direction is indeterminate.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
The FPR2/ALX receptor desensitization documented in is not merely reducing SPM efficacy — it is actively SWITCHING SPM signaling from Gαi-coupled (anti-inflammatory, anti-fibrotic) to β-arrestin-biased (pro-fibrotic) output at the desensitized receptor. β-arrestin-biased FPR2 signaling activates ERK1/2 → SMAD3 crosstalk that synergizes with IRF4/STAT6 at the TGFB1 enhancer, making SPM supplementation in aged desensitized macrophages actively PRO-fibrotic rather than merely ineffective. The Acomys question is irrelevant because the human-specific problem is receptor-level: the same ligand (resolvin D1) produces opposite downstream outputs depending on receptor phosphorylation state.
Testing and possible results
The prediction that would tell it apart
A hypothesis that predicts what its rivals predict is not worth running an experiment over. This is the observation on which this one differs.
In aged human macrophages with documented low FPR2 surface density, resolvin D1 treatment will increase TGF-β1 secretion above untreated controls (not just fail to decrease it), and this increase will be blocked by β-arrestin-2 siRNA but not by pertussis toxin (Gαi inhibitor), confirming β-arrestin-biased signaling as the driver.
States a measurable outcome; comparing rivals needs more conditions. The prediction specifies a secretion increase relative to untreated controls and differential blocking effects under stated conditions. No rival prediction is supplied. A paper already fetched for this hypothesis bears on it.
What testing it would take
The engine's own read on whether this is testable with methods that already exist.
FPR2 surface density by flow cytometry, RvD1 + TGF-β1 ELISA, pertussis toxin and β-arrestin-2 siRNA are all commercially available and protocol-established.
Other explanations
Every other hypothesis the engine wrote for the same gap, and the observation that would separate the two.
In aged human macrophages with documented low FPR2 surface density, resolvin D1 treatment will increase TGF-β1 secretion above untreated controls (not just fail to decrease it), and this increase will be blocked by β-arrestin-2 siRNA but not by pertussis toxin (Gαi inhibitor), confirming β-arrestin-biased signaling as the driver.
- What would separate them
Ageing installs the anti-fibrotic switch that spiny mice are born with predicts: Bisulfite sequencing of the IRF4 half-site CpG at the TGFB1 enhancer in FACS-sorted CD163+ niche macrophages will show >60% methylation in aged (65-75) human donors but <10% in young (20-30) donors, and this methylation will correlate inversely with TGF-β1 secretion upon SPM stimulation in ex vivo polarization assays.
- What would separate them
The fibrosis signal is stopped by the hyaluronan mesh, not by the macrophage predicts: In human niche explant co-cultures, adding exogenous ultra-HMW-HA (>6 MDa) to the macrophage-fibroblast interface will block TGF-β1-driven αSMA expression in fibroblasts even when macrophages are maximally M2-polarized with high TGF-β1 secretion, while low-MW HA (<500 kDa) will permit fibroblast activation at the same TGF-β1 concentration.
- Rival 03 of 04What would separate them
The link between resolving inflammation and fibrosis is an artefact of culture plastic predicts: Human monocyte-derived macrophages polarized with resolvin D1 on 2 kPa polyacrylamide gels will show <2-fold TGF-β1 increase vs. unpolarized controls, while the same cells on tissue culture plastic show >5-fold increase. YAP nuclear/cytoplasmic ratio will correlate with TGF-β1 output (r>0.7) across substrate stiffnesses.
- What would separate them
NAD+ decides whether a healing macrophage also turns fibrotic predicts: Pre-treatment of aged human macrophages with NMN (1mM, 48h) before SPM-driven M2 polarization will reduce TGF-β1 secretion by >50% compared to vehicle, and this effect will be abolished by SIRT6 inhibitor OSS_128167. ChIP-qPCR will show restored H3K9 deacetylation at the TGFB1 promoter in NMN-treated aged macrophages.
What stands behind it
Which of the figures above have a study behind them, which are the engine's own, and what it would take to refute the hypothesis. This audit never judges the idea.
This hypothesis states no figure and cites no study, so there is nothing here to trace.
What it would take to refute it. 6 paper(s) already retrieved for this hypothesis carry its prediction’s terms. Reading them comes before running anything. Already retrieved: Bioactive Anti-Inflammatory Compounds and Therapeutic Strategies for Promoting Resolution.; Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.; From anti-inflammation to pro-resolution: a new paradigm for specialized pro-resolving mediators in regulating neuroinflammation and repair after cerebral ischemia-reperfusion..
6 papers retrieved around this hypothesis
- Specialized Pro-Resolving Mediators at the Ocular Surface: Biosynthesis, Mechanisms, and Therapeutic Potential.PMID 42510749 · full_text · 61,366 characters stored
- From anti-inflammation to pro-resolution: a new paradigm for specialized pro-resolving mediators in regulating neuroinflammation and repair after cerebral ischemia-reperfusion.PMID 42183253 · full_text · 96,346 characters stored
- Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.PMID 41486400 · full_text · 326,603 characters stored
- Bioactive Anti-Inflammatory Compounds and Therapeutic Strategies for Promoting Resolution.PMID 42357303 · full_text · 155,253 characters stored
- The Role of Immunoresolvents in Atherosclerosis: A Mini-Review on Their Biology and Therapeutic Opportunities.PMID 42577494 · full_text · 87,598 characters stored
- Damage-mediated macrophage polarization in sterile inflammation.PMID 37465676 · full_text · 109,932 characters stored
0 citation handles extracted; 1 Europe PMC search run; 8 records examined; 6 sources stored for enrichment, 6 with full text. A citation that did not resolve is a bibliographic failure, not proof that no such paper exists, and no hypothesis is blocked by this audit.