SAMHD1 Research Digest — 2026-08-23¶
Generated by samhd1_monitor | Model: claude-sonnet-5
Summary: 16 papers evaluated | 1 high-relevance (≥7) | 6 medium (5–6) | 9 low (3–4) | 0 scored <3
🔴 High Relevance (Score 7–10)¶
Auto-added to Zotero (threshold ≥6)
Targeting mPTP with NIM811 Alleviates Pancreatic Injury and Inflammatory Response in Severe Acute Pancreatitis (from Gastroenterology/Critical Care (acute pancreatitis))
Feng Dan; Zhang Jia-Rui; Bai Xue; Chen Xia — 2026
Score: 7/10 | Pathways: cGAS-STING, VDAC1, treatment-target, other
Demonstrates mPTP/VDAC-adjacent mitochondrial membrane permeability leading to mtDNA release and cGAS-STING-driven inflammatory cytokine production (IL-1β, IL-6, TNF-α) in a mitochondrial damage model, directly paralleling the BLUE loop mechanism (mtDNA escape → cGAS/STING → IFN-inflammatory output) though in a distinct disease context (pancreatitis) without SAMHD1 involvement.
DOI: 10.21203/rs.3.rs-10616969/v1
🟡 Medium Relevance (Score 5–6)¶
Score ≥6 auto-added to Zotero; lower scores: review manually
The dual role of the cGAS-STING signaling pathway in kidney diseases: from acute injury to chronic fibrosis – molecular mechanisms and precision therapeutic strategies (from Nephrology)
Guangdong Qi; Fei Xue; Hualin Sun; Xinlei Yao; Qingyuan Liu — Frontiers in Pharmacology 2026
Score: 6/10 | Pathways: cGAS-STING, NF-kB-IKK, treatment-target
Reviews cGAS-STING mechanisms (mtDNA leakage, TBK1-IRF3/NF-kB, inflammation-fibrosis) and inhibitor strategies directly relevant to the BLUE loop pathway, though applied to renal disease rather than SAMHD1 context.
DOI: 10.3389/fphar.2026.1882994
Quercetin induces molecular hallmarks of immunogenic cell death and cGAS-STING pathway activation via mitochondrial DNA release in hepatocellular carcinoma cells. (from Oncology/pharmacology)
Lin Tong; Chen Yifan; Huang Zhengrong — Naunyn-Schmiedeberg's archives of pharmacology 2026
Score: 6/10 | Pathways: cGAS-STING, NF-kB-IKK, treatment-target
Demonstrates mtDNA release triggering cGAS-STING-TBK1-IRF3/p65 activation, directly modeling the core Loop A/NF-kB crosstalk mechanism though in an oncology drug-induction context rather than SAMHD1 dysfunction.
DOI: 10.1007/s00210-026-05815-7
Expanding the therapeutic landscape of Still's disease: the emerging role of JAK inhibitors. (from Rheumatology)
Ruscitti Piero; Ursini Francesco; Giacomelli Roberto; Cantarini Luca; Caso Franc — Expert opinion on pharmacotherapy 2026
Score: 6/10 | Pathways: JAK-STAT, NLRP3, treatment-target, clinical-phenotype
Reviews JAK inhibitors modulating IL-1/IL-6/IFN-γ and inflammasome-dependent pathways in Still's disease, directly relevant to the JAK-STAT and NLRP3 nodes and to JAKi therapeutic strategies applicable to the interferon-mitochondrial syndrome, though not SAMHD1-specific.
DOI: 10.1080/14656566.2026.2723582
Mitochondrial DNA in necrosis-like cell death in failing hearts: evidence and mechanisms fostering damage. (from cardiology)
Marciníková Andrea; Jarabicová Izabela; Horváth Csaba; Adameova Adriana — American journal of physiology. Cell physiology 2026
Score: 6/10 | Pathways: cGAS-STING, NLRP3, treatment-target, other
This cardiology-focused review details mtDNA release triggering cGAS-STING and NLRP3/AIM2 inflammasome pathways driving necroptosis/pyroptosis in heart failure, mechanistically overlapping with the BLUE loop (VDAC1/mtDNA/cGAS-STING) and NLRP3 activation streams central to the SAMHD1 disease model, though it does not address SAMHD1 or dNTPase biology directly.
DOI: 10.1152/ajpcell.00266.2026
The Role of Skeletal Muscle Mitochondria in NRLRP3 Inflammasome Signaling (from exercise physiology/skeletal muscle biology)
Jada Sangha; David A. Hood — Biomolecules 2026
Score: 5/10 | Pathways: NLRP3, mito-ROS-NF-kB, treatment-target
Reviews NLRP3 inflammasome activation via mitochondrial DAMPs (ROS, oxidized mtDNA) in skeletal muscle, mechanistically overlapping with the disease's mitochondrial-inflammasome axis but without SAMHD1, cGAS-STING, or IFN-I context, and exercise/myokine focus is only indirectly relevant to ME/CFS fatigue phenotype.
DOI: 10.3390/biom16081218
Systemic effects of gout flares beyond the joints. (from Rheumatology/Cardiology)
Cipolletta Edoardo; Mamas Mamas A; Abhishek Abhishek — Current opinion in rheumatology 2026
Score: 5/10 | Pathways: urate-NLRP3, NLRP3, treatment-target
Discusses gout flare-driven NLRP3/IL-1β activation and cardiovascular sequelae, directly relevant to the GOLD stream (dGTP→uric acid→MSU crystals→NLRP3) and family gout/uric acid phenotype but not tied to SAMHD1 or interferon mechanisms.
DOI: 10.1097/BOR.0000000000001183
🟢 Low Relevance (Score 3–4)¶
Potential specialty bridges — skim titles
Atomic-Level Strain-Engineered Piezoelectric Nanosheets for cGAS-STING Activation. (from materials science/nanomedicine oncology)
Yang Lu; Zang Pengyu; Zhang Rui; Yang Meiqi; Yu Chenghao — 2026
Score: 4/10 | Pathways: cGAS-STING, treatment-target
This paper describes a nanomaterial-based tumor immunotherapy that activates cGAS-STING via mtDNA release, sharing a mechanistic node with the disease's BLUE pathway but in an unrelated oncologic engineering context with no SAMHD1 or interferonopathy relevance.
DOI: 10.1002/anie.5643285
Mitochondrial metabolic remodelling during bacterial infection: Molecular mechanisms, cellular consequences, and therapeutic opportunities. (from Microbiology/Infectious Disease)
Kowalik Agnieszka; Paszenda Patrycja; Frątczak Agnieszka; Piwowar Adrian; Obryck — Tissue & cell 2026
Score: 4/10 | Pathways: cGAS-STING, NLRP3, NF-kB-IKK, mito-ROS-NF-kB
This review covers mitochondrial-immune crosstalk mechanisms (cGAS-STING, NLRP3, ROS-NF-kB, mitochondrial fragmentation) overlapping with the disease's core pathways, but is focused on bacterial infection biology rather than SAMHD1 dysfunction or interferonopathy syndromes.
DOI: 10.1016/j.tice.2026.103873
Gut microbiota–mitochondria–barrier–multiorgan axis: a network-based hypothesis for systemic injury (from Gastroenterology/critical care medicine)
Yachao Li; Huaijue Qiu; Xia Gao; Yanling Zhang; Qin Xia — Frontiers in Immunology 2026
Score: 4/10 | Pathways: cGAS-STING, NLRP3, mito-ROS-NF-kB, other
This paper discusses cGAS-STING and NLRP3 activation via mitochondrial DAMPs in a gut-microbiota-critical illness context, sharing core mechanistic pathways but lacking any SAMHD1, interferonopathy, or family phenotype connection.
DOI: 10.3389/fimmu.2026.1885379
Genome Editing in Primary Mammalian Cells via Electroporation of Editor RNA. (from molecular biology/gene editing methodology)
Maria Viskadourou; J. Workman; Emma V Burke; D. M. Eckley; Johannes Dohr — Journal of visualized experiments : JoVE 2026
Score: 4/10 | Pathways: prime-editing, gene-therapy-delivery
General methods paper on mRNA-based genome editing delivery in primary cells, relevant as generic platform technology for future SAMHD1 correction but not disease-specific or immune/myeloid-focused.
DOI: 10.3791/71449
FGFR4 suppresses antitumor immunity and cuproptosis by disrupting CYLD-mediated stabilization of STING and FDX1. (from Oncology (tumor immunology/cancer therapeutics))
Zhong Hongguang; Huang Ruixuan; Deng Wenyuan; Ruan Ruiwen; Dai Xiaofeng — 2026
Score: 4/10 | Pathways: cGAS-STING, treatment-target, other
This paper involves cGAS-STING pathway regulation via CYLD/FDX1/cuproptosis in cancer immunotherapy, but is oncology-focused with no connection to SAMHD1, dNTP metabolism, or interferonopathy mechanisms central to this disease profile.
DOI: 10.1016/j.canlet.2026.218790
Epithelial interferon-stimulated gene programs modulate chemotherapy sensitivity in colorectal cancer via EPSTI1. (from Oncology)
Erkan Erdogan Pekcan; Hämäläinen Emmi; Kolikova Julia; Nikupaavola Tiia; Sajnani — Oncogene 2026
Score: 4/10 | Pathways: JAK-STAT, treatment-target
Discusses JAK-STAT/ISG program and ruxolitinib in a colorectal cancer oncology context, tangentially touching interferon signaling but without SAMHD1, mitochondrial, or innate immune inflammasome mechanisms central to the disease profile.
DOI: 10.1038/s41388-026-03957-9
Dysfunction of the Neurovascular Unit in Diabetic Retinopathy: Advances from Molecular Mechanisms to Targeted Interventions. (from Ophthalmology)
Zhao Chunning; Qin Leilei; Zhang Jing; Wang Xiu — Stem cell reviews and reports 2026
Score: 3/10 | Pathways: NLRP3, other
This is a diabetic retinopathy review touching on NLRP3/mitochondrial dysfunction in a generic ophthalmology context, without any SAMHD1, interferon, or family-phenotype linkage.
DOI: 10.1007/s12015-026-11213-6
Alopecia Areata: Current and Emerging Therapies. (from Dermatology)
Domingues João; King Brett; Torres Tiago — Drugs 2026
Score: 3/10 | Pathways: JAK-STAT, treatment-target
Reviews JAK inhibitors (baricitinib) for alopecia areata, relevant as a JAK-STAT therapeutic class overlapping with interferonopathy management but not directly tied to SAMHD1 mechanism or family phenotypes.
DOI: 10.1007/s40265-026-02371-5
Integrated Multi-omics Reveals CDKN1A Suppression and Metabolic Regulation as Key Mechanisms of Huangqi Guizhi Wuwu Decoction Against Doxorubicin-Induced Cardiotoxicity. (from Cardio-oncology/pharmacology (traditional Chinese medicine))
Hou Qian; Yu Xinyue; Wu Ke; Chen Siling; Mao Xin — Cardiovascular toxicology 2026
Score: 3/10 | Pathways: ISG15-mitophagy, other
This paper on a Chinese herbal decoction mitigating doxorubicin cardiotoxicity incidentally identifies Irf7/Isg15 and apoptosis genes (Bax, Cdkn1a) but has no mechanistic connection to SAMHD1, interferonopathy, or the core inflammasome/mitochondrial pathways central to this disease profile.
DOI: 10.1007/s12012-026-10168-x
Pathway Coverage This Week¶
treatment-target: 11 paperscGAS-STING: 8 papersNLRP3: 7 papersother: 6 papersNF-kB-IKK: 3 papersJAK-STAT: 3 papersmito-ROS-NF-kB: 3 papersVDAC1: 1 papersclinical-phenotype: 1 papersurate-NLRP3: 1 papersprime-editing: 1 papersgene-therapy-delivery: 1 papersISG15-mitophagy: 1 papers