SDF-1, Stem Cell Mobilisation, and the Fibrinaloid Phenotype: A Curated Source List

Table of Contents

Declaration of Purpose

This is a source-curated companion to the main Amyloid Fibrin Microclots review. It exists to hold the SDF-1 / CXCL12 and stem-cell mobilisation literature in one place, plus archived media assets relevant to the topic. Claims carry evidence tags under the system documented on the Methodology page. Not medical advice.

What this page is for

The main Amyloid Fibrin Microclots review covers the mechanism, the patient-cohort detection, the Edogawa clinical pathway, and the treatment landscape in depth. This page covers the adjacent literature that the main review references but does not expand on:

SDF-1 / CXCL12 as a stem-cell mobilisation axis with a documented role in amyloid clearance in preclinical models.
Bone-marrow and dental-pulp mesenchymal stem cells (BM-MSC, SHED) as sources of regenerative secretomes with anti-inflammatory and pro-repair activity.
Ischaemia-reperfusion injury as the link between fibrinaloid microvascular obstruction and tissue-level pathology.
Spike-fibrinogen binding as the upstream trigger.

It also preserves the curated paper list and media archive that previously lived here, with citation details corrected to canonical form.

The SDF-1 / CXCL12 axis

SDF-1 (stromal-cell derived factor-1, also called CXCL12) is a chemokine that mobilises CXCR4-positive cells from bone marrow. It is best known for its role in haematopoietic stem-cell trafficking, but the same axis has been studied in neurodegeneration because CXCR4 is expressed on microglia and several neural cell populations.

Key peer-reviewed finding. In a rat model of Alzheimer's disease, combination of SDF-1 with G-CSF (granulocyte colony-stimulating factor) reduced amyloid-beta plaque burden, lowered apoptosis markers, and improved cognition, with the proposed mechanism being microglial mobilisation and M1-to-M2 polarisation. [AN] CONFIDENCE: MODERATE for the preclinical effect; no human replication in the PASC / spikeopathy context.

This is the axis that connects the SDF-1 / stem-cell literature to the fibrinaloid microclot literature: if fibrinaloid clots are driving microvascular obstruction and secondary ischaemia-reperfusion injury (see below), then endogenous repair requires both clearance of the clots and mobilisation of regenerative cells. SDF-1 sits on the mobilisation side; DFPA (double filtration plasmapheresis) sits on the clearance side.

Source: SDF-1 + G-CSF in rat AD model, PMC8924615.

Mesenchymal stem cells and the secretome angle

Two MSC sources dominate this literature:

Bone-marrow MSCs (BM-MSCs). Documented to inhibit neuroinflammation, shift microglia from M1 to M2 phenotype, and reduce amyloid-beta and tau burden in AD models. The effect is largely paracrine (mediated by secreted factors) rather than through cell replacement. [AN + SR] CONFIDENCE: MODERATE for the mechanism; limited human translation in neurodegeneration.

Sources: BM-MSC mechanisms in AD, PMID 34566422; HP-BMSCs post-CPR, PMID 37246833; Stem cells in neurodegeneration review, PMC3025439.

SHED (Stem cells from Human Exfoliated Deciduous Teeth). A well-characterised dental-pulp MSC source whose conditioned medium contains IL-10, BDNF, NGF, VEGF, and IGF-1. This is the secretome used in the Edogawa Hospital clinical pathway as regenerative support after DFPA. The terminology matters here: what McCairn / Edogawa call "SGF" or "SCGF" informally is SHED-conditioned medium, not isolated Stem Cell Growth Factor / CLEC11A (a single specific cytokine). See the main review's Edogawa Clinical Pathway section for the full discussion.

Sources: El Moshy 2020 SHED-CM review, PMID 32089709; de Cara 2019 angiogenic properties, Heliyon; Engineered MSCs in ischemia, PMC11554727.

Fibrinaloid microclots and ischaemia-reperfusion injury

The ischaemia-reperfusion (I/R) angle is what links fibrinaloid microvascular obstruction to tissue-level damage. The chain is straightforward:

Fibrinaloid microclots obstruct capillaries and precapillary arterioles.
Downstream tissue experiences hypoxia (ischaemia).
If perfusion is restored (either spontaneously or via fibrinolysis), the re-oxygenation generates reactive oxygen species, complement activation, and calcium overload in the previously ischaemic tissue.
The resulting inflammatory and oxidative damage is often worse than the ischaemia itself.

This is the textbook I/R injury mechanism applied to the fibrinaloid context. The Pretorius / Kell group formalised the connection in a 2022 Biochemical Journal paper, arguing that fibrinaloid-driven microvascular obstruction creates the conditions for chronic, low-grade I/R injury across multiple vascular beds. [SR + MECHANISTIC] CONFIDENCE: MODERATE .

Source: Kell & Pretorius 2022 on I/R in Long COVID, Biochem J 479:1653.

Spike, fibrinogen, and the prion interface

Two peer-reviewed threads are relevant here.

Spike binds fibrinogen directly. Ryu et al. (2024, Nature) localised the binding site on the fibrinogen alpha chain and showed the interaction is necessary for much of spike's thromboinflammatory effect in mouse models. [PR] CONFIDENCE: HIGH . This is the upstream event that makes the fibrinaloid story coherent: spike exposure shifts fibrin toward the amyloid-like, fibrinolysis-resistant state.

Source: Ryu et al. 2024, Nature.

Fibrinogen interacts with prion protein (PrP). A separate literature documents that fibrinogen mitigates PrP toxicity and PrP stabilises clot structure. This is a two-way interface between clotting biology and prion-related biology, and is one of the reasons the fibrinaloid story overlaps with prion-like and CJD discussions in the broader literature.

Source: Fibrinogen-prion interactions, PMC8977893.

For the prion-like acceleration claims specific to spike (Wang 2024 on amyloid-beta acceleration, Nystrom 2022 on alpha-synuclein), see the main review's Amyloid cross-seeding section.

Curated source list

All citations below are in canonical form (PubMed / PMC / publisher DOI). The table is the persistent part of this page; the prose above interprets the most important rows.

Paper	Title / Topic	Takeaway	Relevance
PMC8924615	SDF-1 + G-CSF in rat AD model	Combo reduced amyloid-beta plaques and apoptosis; improved cognition via microglial mobilisation	Direct amyloid-beta reduction; stem-cell mobilisation
PMC3025439	Stem cells in neurodegeneration	Trophic and repair effects beyond cell replacement	Supports repair mechanisms despite plaques
PMID 34566422	BM-MSC mechanisms in AD	Inhibits neuroinflammation; shifts microglia M1 to M2; reduces amyloid-beta and tau	Targets inflammatory drivers
PMID 37246833	HP-BMSCs post-CPR	Suppresses pyroptosis and ROS-driven inflammation	Indirectly favours clearance
PMC9543648	Stem-cell angiogenesis and wound healing	Angiogenesis and extracellular vesicles improve repair	Vascular repair aids clearance
PMC11554727	Engineered MSCs in ischemia	eMSCs and their EVs reduce infarct size; boost repair	Applicable repair pathways
PMID 32089709	El Moshy 2020 SHED-CM review	Dental-pulp MSC secretome composition established (IL-10, BDNF, NGF, VEGF, IGF-1)	Direct bearing on Edogawa SHED-CM component
Heliyon 5:e01560	de Cara 2019 SHED-CM angiogenesis	SHED-conditioned medium promotes endothelial proliferation, migration, VEGF production	Mechanistic support for SHED-CM regenerative use
Biochem J 479:1653	I/R injury in Long COVID	Microclot-hypoxia loop; targets ROS, iron, clot burden	Connects fibrinaloid clots to tissue damage
Biochem J 479:537	Kell & Pretorius 2022 fibrinaloid review	Formalises fibrinaloid microclots as the PASC clot phenotype	Names the clinical entity
Nature 2024	Ryu et al. spike-fibrinogen binding	Crystallised binding site; antibody 5B8 blocks effect	Upstream cause of fibrinaloid transformation
PMC8977893	Fibrinogen-prion interactions	Fibrinogen mitigates PrP toxicity; PrP stabilises clots	Prion / amyloid clot interface
Vaccines 11(7):1139	COVID and amyloidosis review	Serum amyloid A / inflammation link; case reports	Pro-amyloid inflammatory context
PMC8456430	COVID-related amyloidogenesis	Inflammatory-driven amyloid formation context	Background mechanism
PMID 35579205	Spike and amyloidogenesis	Mechanistic overlap	Background
PMID 36362302	Fibrinaloid microclots in POTS / Long COVID	Documents microclot presence in PASC subsets	Patient-cohort evidence

Archived media assets

These are preserved from the original version of this page because they carry provenance value for the topic. Most document researcher communications or reference slides; none are primary data.

Images:

/media/amyloid/kevin-jihad-science.jpg - stylised avatar associated with Kevin McCairn PhD. Retained for historical provenance; this page no longer treats McCairn as the central node of the topic (see the main review for the current framing).
/media/amyloid/mccairn-broadcast.jpg - locally archived frame from a McCairn stream (permission granted by the source).
SDF-1 / amyloid reference slide.
McCairn broadcast card on fibrin pathology.
Micrograph illustrating microclot morphology.

Video:

Microclot morphology short clip.

External links (papers, streams, archived commentary)

Papers (canonical sources only):

Archived commentary (not peer-reviewed):

McCairn 2025, post-gestational case report, Substack. [INV] CONFIDENCE: LOW .
Ethical Skeptic, "Houston we have another problem" (2025). Investigator commentary; not peer-reviewed.

Archived streams (commentary, not primary data):

Rumble: Environmental super-prion risk assessment pt. 2 with Colm Kelleher
Rumble: "And then they came for the children 3: amyloid kill shots"
YouTube: long-form discussion

Amyloid Fibrin Microclots in Long COVID: Evidence Review and Treatment Landscape - the main review this page companions.
The Spikeopathy Research Cluster - the unifying clearance-and-tolerance framework.
The Slow Burn, Part 1: Spike Persistence and Microclots.
Methodology - how this article's evidence tags work.