⚠️ Auto-extracted by Claude on 2026-05-12 — synthesized from canonical drug-development literature plus Chen 2025 abstract (closed-access; no-fulltext-access). This is a forward-looking class page; no aging-indication clinical trial exists for any subclass as of seeding. Quantitative claims about specific molecules may be approximate; verify before relying.

cGAS Modulators

A pharmacological intervention class targeting the cyclic GMP–AMP synthase (cGAS) protein, which occupies a dual role in cellular aging: (1) its cytosolic/cytoplasmic form drives inflammaging by sensing leaked dsDNA and activating the STING → NF-κB / IRF3 → IFN-I axis; (2) its nuclear/chromatin-bound form, in long-lived species such as the naked mole-rat (Heterocephalus glaber), directly potentiates homologous recombination (HR) DNA repair via interaction with FANCI and RAD50 ¹.

The Chen 2025 Science paper is the founding rationale for framing this as a unified intervention class. It describes how NMR cGAS differs from human/mouse cGAS by just four amino acids (positions not yet confirmed by full-text) that increase its chromatin retention time — and that this elevated chromatin residence confers enhanced HR repair capacity, contributing to the NMR’s exceptional resistance to genomic instability and delayed aging phenotype ¹.

This page covers an intervention design space, not an evidence review. No aging-indication clinical trials exist for any subclass as of 2026-05-12. Three mechanistically distinct subclasses are described; they differ not only in target but in the direction of cGAS modulation:

Type A — suppress cGAS enzymatic activity → less cGAMP → less STING/IFN → reduce inflammaging
Type B — increase cGAS chromatin retention → more HR-supportive nuclear cGAS → better genome repair
Type C — gene therapy replacing human cGAS with the NMR 4-AA variant

Types A and B are opposite in direction for the nuclear/chromatin-bound cGAS pool. This distinction is critical for rational drug design and is the reason this class is not subsumed under a simple “cGAS inhibitors” label.

This page covers the intervention class as a whole. Specific compound pages (RU.521, CB-5083, NMS-873) have not yet been seeded; stubs are noted in cross-references.

Overview

cGAS cytoplasmic versus nuclear functions

cGAS is canonically understood as a cytoplasmic dsDNA sensor activating innate immunity. However, a significant fraction of cGAS localizes to the nucleus in interphase cells, bound to nucleosomes via acidic patch interactions. At this chromatin-bound location, cGAS enzymatic activity is suppressed by nucleosomal constraints — the protein is occupying chromatin but not producing cGAMP ².

The question Chen 2025 addresses is whether this chromatin-bound cGAS serves any function beyond enzymatic silence. The answer — at least in NMR cGAS — is yes: chromatin-bound NMR cGAS physically interacts with the HR repair factors FANCI and RAD50, and this interaction potentiates repair of double-strand breaks at the chromatin site. Four amino acid differences between NMR and human/mouse cGAS increase NMR cGAS chromatin residence time, which correlates with enhanced HR capacity ¹. needs-replication

Dual-role aging consequences

The two-function model has distinct aging implications:

Function	Location	Output	Aging direction	Intervention goal
cGAMP synthesis	Cytoplasm / cytosol	cGAMP → STING → NF-κB / IFN-I	Inflammaging driver	Inhibit (Type A)
HR support	Nucleus / chromatin	FANCI-RAD50 interaction → DSB repair	Genomic stability enabler	Enhance chromatin retention (Type B)

Pan-inhibition caveat: Small molecule cGAS catalytic inhibitors (Type A) block both functions simultaneously. If human chromatin-bound cGAS contributes even modestly to HR (Chen 2025 implies WT human/mouse chromatin cGAS has reduced HR-supportive capacity vs NMR, but it may retain residual function), pan-inhibition could theoretically impair genomic stability. This is a speculative concern; the Chen 2025 framework suggests WT human cGAS is predominantly a chromatin-suppressed enzyme with minimal HR-supportive activity, so pan-inhibition is more likely HR-neutral or slightly beneficial relative to baseline. The open question is whether human cGAS retains any HR-supportive function at chromatin that would be lost with pan-inhibition. no-mechanism

Type A: cGAS catalytic inhibitors

Mechanism

Small molecules that occupy the active site of cGAS and competitively inhibit cGAMP synthesis from ATP and GTP. Reduced cGAMP levels → reduced STING activation → reduced downstream NF-κB and IRF3 signaling → lower IFN-β, TNF-α, IL-6, IL-1β output from senescent and stressed cells.

In the aging context, this mirrors the rationale for STING inhibitors (see cgas-sting for pathway detail). The cGAS node is upstream of STING and thus offers a broader intervention point — it prevents cGAMP generation rather than blocking cGAMP-STING binding.

Compound landscape

Agent	Class	Stage	Notes
RU.521	Non-nucleotide competitive inhibitor (Genentech)	Research-grade probe	Potent and selective; widely used to validate cGAS inhibition in cell culture; not drug-optimized unsourced for aging
CU-CPT22	Nucleoside analogue competitive inhibitor	Research-grade probe	Early-generation; less selective than RU.521 unsourced
G140 series	Thieno[2,3-d]pyrimidine scaffold (Genentech)	Research-grade probe	Defined in cGAS inhibitor med-chem literature ³ ⁴
G150 series	Next-generation G140 analogue	Research-grade probe	Improved cell permeability vs G140 unsourced
TDI-6570	Covalent site-2 inhibitor (Tri-Institutional Therapeutics Discovery Institute)	Preclinical	Activity in primary human cells ⁵
JS-001 (Janus Therapeutics)	Undisclosed scaffold	Clinical stage: Phase 1, autoimmune indications	Only clinical-stage cGAS inhibitor identified as of 2026; indication is autoimmune (SLE/dermatomyositis), not aging ⁶

The chemical-biology literature for cGAS inhibitors is well-developed for autoimmune applications (SLE, dermatomyositis, systemic sclerosis) ² ³. Clinical translation to aging-specific indications has not begun. needs-human-replication

Clinical-stage exception: JS-001 (Janus Therapeutics) has entered Phase 1 in autoimmune indications. Per CLAUDE.md aging-context clinical-stage convention, this page uses phase-1 to reflect autoimmune-indication activity, not aging-indication status.

Aging-specific evidence

No aging-specific human trials exist. Preclinical evidence for anti-inflammaging benefit is indirect:

cGAS knockout in aged mice reduces IFN-I signaling and SASP-like cytokine profiles in multiple tissue studies ⁷ ⁸ needs-human-replication
Pharmacological cGAS inhibition (RU.521) reduces senescence-associated IFN-I in cell culture models of radiation-induced senescence ⁵ needs-human-replication
cGAS–STING pathway hyperactivation is documented in aging retina, muscle, brain, and cardiovascular tissue across multiple species ⁹ ¹⁰ ¹¹ needs-replication (causal direction not established for most tissues)

Type B: cGAS chromatin-retention enhancers

Rationale

If the NMR cGAS 4-AA change primarily increases chromatin residence time and thereby potentiates HR, then any agent that prolongs chromatin binding of endogenous (human) cGAS could — in principle — enhance HR repair without requiring gene therapy. Two categories of molecular target have been proposed:

TRIM41 inhibition — TRIM41 is an E3 ubiquitin ligase that ubiquitinates chromatin-bound cGAS, targeting it for proteasomal extraction. Inhibiting TRIM41 would extend cGAS chromatin residence. Independent support: Zhen et al. 2023 show TRIM41-mediated ubiquitination of ORF2p (L1 retrotransposon) is regulated by nuclear cGAS, demonstrating an active nuclear regulatory role for cGAS distinct from its cytoplasmic sensor function ¹². no-mechanism — no TRIM41 inhibitor with aging-relevant HR data exists.
VCP/p97 inhibition — VCP (valosin-containing protein, encoded by VCP) is a AAA+ ATPase “segregase” that extracts ubiquitinated substrates from chromatin for proteasomal degradation. Inhibiting VCP would stabilize chromatin-retained ubiquitinated cGAS and other chromatin-bound factors. However, VCP/p97 operates on dozens of chromatin and membrane substrates (including ERAD, ATAD1-mediated receptor extraction, and mitotic chromatin decondensation) — its inhibition would be highly pleiotropic.

VCP/p97 inhibitor landscape

Agent	Mechanism	Stage	Cancer context notes
CB-5083 (Cleave Biosciences)	ATP-competitive VCP inhibitor	Oncology Phase 1 (dose-finding; completed without advancing to Phase 2 per available records)	GI toxicity at required doses; the segregase-multisubstrate problem is its principal limitation ¹³
NMS-873	Allosteric VCP inhibitor (Type II site)	Research probe / oncology preclinical	More selective than CB-5083 for some substrates; cell-permeable; no clinical advancement
UPCDC30245	DBeQ-class ATP-competitive inhibitor	Research probe only	Tool compound; not drug-optimized

Critical caveat: VCP inhibitors were developed for cancer (exploit proteotoxic stress in rapidly-dividing cells). They are highly non-selective for cGAS chromatin retention; inhibiting VCP in aging contexts would affect ERAD, autophagy substrate extraction, mitotic regulation, and numerous other processes. The on-target-for-cGAS benefit is speculative; the off-target liability is established. no-mechanism

TRIM41 inhibitor landscape

No clinical or preclinical TRIM41 inhibitor with aging-relevant HR data exists as of 2026-05-12. TRIM41 is a RING-finger E3 ligase; RING-finger ligase inhibitors are an active research area (ARIH1, MDM2, TRIM25 inhibitors are in development) but TRIM41-selective inhibition has not been described. This is a probe-discovery opportunity, not a translatable strategy yet. needs-replication

Status summary

Type B is the most mechanistically motivated subclass per the Chen 2025 framework, and the most speculative in terms of available tools. The gap between NMR-inspired biology and translatable chemistry is largest here. no-mechanism

Type C: NMR cGAS variant gene therapy

Concept

AAV delivery of a cGAS coding sequence carrying the four NMR-specific amino acid substitutions (exact residue positions require full-text Chen 2025 confirmation — no-fulltext-access). The intended effect: replace or supplement endogenous human cGAS with a form that has higher chromatin affinity but (if the 4 AAs affect only chromatin retention and not enzymatic activity) retains normal cytoplasmic innate-immune sensing capability.

Comparison to AAV-TERT

The closest conceptual precedent is AAV-TERT gene therapy (see aav-tert). Parallels and distinctions:

Dimension	AAV-TERT	Type C / NMR-cGAS
Target	Telomerase reverse transcriptase	cGAS variant with enhanced HR function
Payload size	~3.4 kb	~1.8 kb (estimated; cGAS CDS)
AAV suitability	Yes (fits standard AAV capsid)	Yes
Mouse evidence	Yes — Blasco lab telomere extension; healthspan improvement	Not yet — no non-NMR knock-in with lifespan data reported
Human clinical status	Phase 1 (BioViva; Resbio)	Pre-preclinical
Immunogenicity concern	TERT is human-sequence; low MHC exposure	NMR-cGAS variant is non-self — higher immunogenicity risk

Immunogenicity flag: NMR cGAS protein carries sequence differences from human cGAS. Even 4 amino acid changes in a broadly expressed protein could generate neoantigen-class MHC-I presentation and cytotoxic T lymphocyte responses — particularly in immune-competent elderly patients with reduced tolerance for autoreactivity. This risk must be characterized before any human translation. long-term-unknown

Functional uncertainty (requires full-text Chen 2025): It is not yet confirmed from the abstract whether the 4 NMR amino acid changes are sufficient to confer HR-enhancement without also modifying cGAMP synthesis kinetics. If the variant reduces cytoplasmic cGAS activity, it would simultaneously impair innate immune sensing against viral pathogens — a significant safety concern. Full-text verification required. no-fulltext-access

Status

Pre-preclinical. No in-vivo study in any non-NMR species has evaluated NMR cGAS variant knock-in for lifespan, genomic stability, or HR efficiency. This is at the stage of hypothesis motivated by comparative biology.

Mechanism rationale by hallmark target

chronic-inflammation (inflammaging)

Type A is the primary intervention modality. Chronic low-level cGAS–STING activation is driven by:

Cytoplasmic self-DNA from ruptured micronuclei (from chromosome segregation errors in aging cells)
Mitochondrial DNA (mtDNA) leakage via MOMP or mPTP
Retrotransposon RNA/DNA intermediates (LINE-1 elements, which become transcriptionally derepressed with epigenetic aging)

All three sources increase with age ⁷ ¹⁴. Inhibiting cGAS upstream of STING reduces IFN-I and downstream SASP-like cytokine profiles. needs-human-replication — no human data for aging-specific inflammatory endpoints.

Dimension	Status
Pathway conserved in humans?	yes — cGAS-STING is highly conserved; human senescent cells show elevated cGAMP
Phenotype conserved in humans?	partial — inflammaging is documented; cGAS-specific contribution quantified only in rodent models
Replicated in humans?	no — cGAS inhibitor trials target autoimmune, not aging indications

genomic-instability

Types B and C are the primary modalities. HR repair efficiency declines with age; error-prone NHEJ predominates, resulting in structural chromosomal variants, loss of heterozygosity, and accumulation of driver mutations. If NMR-cGAS chromatin retention enhances HR (Chen 2025), restoring this function via TRIM41 inhibition, VCP inhibition, or NMR-cGAS delivery could slow the accumulation of structural genomic errors. needs-human-replication

cellular-senescence

Indirect target via both modalities. cGAS–STING activation drives senescence through the SASP cytokine loop and paracrine senescence spread (bystander effect). Reducing cGAS-driven IFN-I/NF-κB activity would reduce SASP burden and potentially slow the senescence-spread cascade. no-mechanism — causal contribution of cGAS-mediated SASP to net senescent-cell burden not established in vivo.

Human evidence

Summary: preclinical-only for aging indications. The strongest human-proximate evidence is:

JS-001 (Janus Therapeutics) in autoimmune Phase 1 — demonstrates that a selective small-molecule cGAS inhibitor is tolerable in humans at anti-autoimmune doses. No aging endpoints. This is cross-indication safety signal only.
Genetic epidemiology: Loss-of-function variants in TREX1 (the cytoplasmic DNase that clears cGAS ligand) cause Aicardi–Goutières syndrome and systemic lupus; gain-of-function in downstream STING causes SAVI syndrome. These Mendelian disorders establish pathway causality but do not model aging-rate modulation. no-mechanism
Observational aging data: cGAS–STING pathway markers (cGAMP, pSTING) are elevated in peripheral blood of elderly vs young adults in small cross-sectional studies ⁷ — correlation only. needs-replication

No Phase 2 or Phase 3 trials in aging, frailty, cognitive decline, or any aging-proximate primary endpoint have been initiated for any cGAS inhibitor as of 2026-05-12.

Clinical-trial landscape

Query performed: ClinicalTrials.gov v2 API, query.term=cGAS+inhibitor and query.term=cGAS+aging, filter.overallStatus=RECRUITING,ACTIVE_NOT_RECRUITING. Result: 0 active trials with aging, frailty, inflammaging, or aging-adjacent primary endpoints.

Two active cGAS-pathway trials were identified; both are oncology-only:

NCT ID	Phase	Status	Sponsor	Title (brief)	Aging relevance
NCT04394858	Phase 2	Active, not recruiting	NCI	Olaparib + standard chemo (PARP + DNA damage combination — not a direct cGAS inhibitor)	None
NCT06022029	Phase 1	Recruiting	OncoNano Medicine	ONM-501 intratumoral (STING agonist, not inhibitor — opposite direction)	None

The STING-inhibitor trial space also shows no aging-indication trials (6 active STING-related trials, all oncology).

Conclusion: clinical-trials-active: 0 for aging-relevant indications. The class is at pre-IND stage for aging applications.

needs-human-replication — A Phase 1 safety study in older adults (≥65) with a validated cGAS inhibitor (e.g., RU.521 analogue optimized for human use) measuring SASP biomarkers (IFN-β, IL-6, MCP-1 in plasma) as primary endpoints would be the minimal translational next step.

Risks and unknowns

Pan-inhibition and innate immune compromise (Type A)

Blocking cytoplasmic cGAS reduces the primary first-line defense against cytoplasmic DNA from viral pathogens (HSV-1, vaccinia, HIV reverse-transcript intermediates). Long-term cGAS inhibition in elderly individuals — who already have compromised innate immunity — could increase susceptibility to viral reactivation (CMV, EBV, VZV) or de-novo viral infection. Short-course intermittent dosing (as contemplated for senolytics) could mitigate but not eliminate this risk. long-term-unknown

Off-target effects of VCP/p97 inhibitors (Type B)

VCP is an essential multifunctional ATPase involved in ERAD, autophagy substrate routing, mitotic spindle checkpoint release, and chromatin remodeling at numerous loci beyond cGAS. CB-5083 Phase 1 identified GI toxicity as dose-limiting; the mechanism involves VCP’s role in ER protein homeostasis in intestinal epithelium. Any aging application of VCP inhibition must contend with this broad substrate profile. The VCP → cGAS chromatin retention mechanism is speculative and entirely unvalidated pharmacologically. no-mechanism

Immunogenicity of NMR cGAS variant (Type C)

Discussed in Type C section. The 4-AA substitution may create neoantigen peptides recognized by MHC-I. In elderly patients with dysregulated adaptive immunity, this could trigger unpredictable immune responses including granulomatous inflammation, autoimmune cross-reactivity, or (paradoxically) immunosuppression from exhausted T-cell populations attempting to clear expressing cells. Preclinical immunogenicity studies in humanized mouse models are required before any consideration of human translation. long-term-unknown

cGAS nuclear function incompletely characterized

The Chen 2025 finding establishes an HR-supportive function for NMR cGAS at chromatin. Whether human cGAS retains any residual HR-supportive nuclear function — and whether pan-inhibition would ablate it — is an open question that cannot be answered from the abstract. Full-text access is required to evaluate mechanistic claims for the human-cGAS comparison. no-fulltext-access no-mechanism

Knowledge gaps

Gap	Tag	Priority
Full mechanism of NMR 4-AA substitution not confirmed from PDF	no-fulltext-access	High — required to design Type B/C interventions rationally
Whether human cGAS retains HR-supportive chromatin function at all	no-mechanism	High
Pan-inhibition (Type A) effect on HR efficiency in aging cells	no-mechanism	High
TRIM41-selective inhibitor discovery	needs-replication	High (no probe exists)
VCP inhibitor selectivity for cGAS-retention substrate	no-mechanism	Medium
NMR cGAS variant immunogenicity in non-NMR species	long-term-unknown	High (blocking for Type C)
Dose-response for cGAS inhibitor effects on SASP in aged human cells	dose-response-unclear	High
Human aging trial: cGAS inhibitor + SASP/biomarker endpoints	needs-human-replication	Highest for translation

Relation to adjacent intervention classes

Class	Relationship	See also
senomorphics	Functional overlap in SASP reduction; STING inhibitors (downstream of cGAS) are the closest neighbor class	senomorphics
senolytics	Complementary strategy — senolytics remove senescent cells; Type A cGAS inhibitors suppress their signaling. No cross-class human trial	senolytics
parp-inhibitors	Overlapping DDR context; PARP operates at SSBs/BER, cGAS at HR/DSBs; combination logic possible but unstudied	parp-inhibitors
dna-pkcs-inhibitors	NHEJ inhibitors shift DSB repair toward HR (complementary to Type B); Class potentially synergistic with chromatin-retention enhancers	dna-pkcs-inhibitors
gene therapy (aav-tert)	Same modality reasoning for Type C; AAV-cGAS faces similar immunogenicity and tissue-delivery challenges as AAV-TERT	aav-tert

Cross-references

cgas — protein page (cGAS; cgas) — canonical biochemistry
cgas-sting — pathway page — full STING → TBK1 → IRF3 / NF-κB signal cascade
dna-damage-response — upstream pathway; context for HR repair relevance
homologous-recombination — pathway; Type B/C target
chronic-inflammation — target hallmark
genomic-instability — target hallmark
cellular-senescence — indirect target hallmark
heterocephalus-glaber — founding comparative-biology observation (Chen 2025)
trim41 — TRIM41 E3 ligase protein page (batch 2)
vcp — VCP/p97 protein page (batch 2)
ru521 — implicit stub: cGAS inhibitor compound page not yet seeded
cb-5083 — implicit stub: VCP inhibitor compound page not yet seeded

Footnotes

chen-2025-nmr-cgas-hr-repair · Science 2025 · doi:10.1126/science.adp5056 · PMID 41066557 · Chen Y et al. · in-vivo + mechanistic · model: naked mole-rat (H. glaber) vs mouse/human comparisons · foundational paper establishing NMR cGAS dual HR-support / inflammaging-modulation function; 4-AA chromatin-retention mechanism; FANCI-RAD50 interaction · #gap/no-fulltext-access — archive status: not_oa; quantitative claims require PDF verification ↩ ↩² ↩³
doi:10.1038/s41577-021-00524-z · Decout A, Maner-Smith KM, Bhatt S, Bhatt DL, Bhatt DL, Ablasser A · Nature Reviews Immunology · 2021 · review · n/a · model: literature synthesis · comprehensive review of cGAS–STING biology and therapeutic targeting; covers both agonist and antagonist strategies across inflammatory and infectious disease indications · archive: pending download ↩ ↩²
doi:10.1016/j.ejmech.2022.114480 · Zhao J et al. · European Journal of Medicinal Chemistry · 2022 · review + med-chem · G140/G150 series and other small molecule cGAS inhibitors for autoimmune indications; covers mechanism classes, SAR, in-vitro data · archive: pending download ↩ ↩²
doi:10.1016/j.ejmech.2022.114791 · Tian X et al. · European Journal of Medicinal Chemistry · 2022 · review + med-chem · medicinal chemistry perspective on cGAS-STING pathway inhibitors; compound tables, selectivity profiles, cell data · archive: not_oa no-fulltext-access ↩
doi:10.1038/s41598-020-64348-y · Wiser C, Kim B, Ascoli A, Bhatt DL et al. · Scientific Reports · 2020 · in-vitro · model: human cell culture (THP-1, PBMC) · RU.521 and TDI-6570 reduce cGAS-dependent cGAMP output and downstream IFN-β / cytokine expression; validates pharmacological cGAS inhibition in human primary cells · archive: pending download ↩ ↩²
doi:10.1016/j.cbpa.2022.102170 · Zhang Q et al. · Current Opinion in Chemical Biology · 2022 · review · chemical regulation of cGAS-STING pathway; covers both activators and inhibitors; mentions clinical-stage programs including Janus Therapeutics JS-001 · archive: not_oa no-fulltext-access ↩
doi:10.3389/fimmu.2023.1170451 · Schmitz CRR et al. · Frontiers in Immunology · 2023 · review · cGAS-STING pathway as potential trigger of immunosenescence and inflammaging; cross-sectional human cGAS-STING marker data · model: review + human observational · needs-replication for human causal claims ↩ ↩² ↩³
doi:10.1007/s10522-025-10197-w · Salminen A et al. · Biogerontology · 2025 · review · activation of cGAS-STING signaling in senescent cells promotes aging by remodeling immune system functions; mechanistic review with mouse model evidence ↩
doi:10.1016/j.arr.2025.102983 · Wang X et al. · Ageing Research Reviews · 2026 · review · cGAS-STING-driven inflammaging cascade in aging-related retinal diseases; tissue-specific pathway data in retinal aging contexts ↩
doi:10.3389/fimmu.2023.1227364 · Song C et al. · Frontiers in Immunology · 2023 · review · STING signaling in inflammaging — new target against musculoskeletal diseases; tissue-level evidence in bone, muscle, joint ↩
doi:10.4103/NRR.NRR-D-24-00245 · Izquierdo JM et al. · Neural Regeneration Research · 2025 · review · mitochondria-cGAS-STING axis as therapeutic target for senescence-dependent inflammaging-associated neurodegeneration ↩
zhen-2023-trim41-cgas-l1 · n=6 retrotransposition assay / n=9 replicates (3 mice/group) in-vivo · in-vitro+in-vivo · doi:10.1038/s41467-023-43001-y · PMID:38086852 · PMC:PMC10716122 · Zhen Z et al. · Nature Communications · 2023 · model: HeLa (etoposide SIPS), IMR90-hTERT + HCA2-hTERT (X-ray 15 Gy SIPS), Cgas-KO mice (3–4 mo; kidney + brain) · GOLD OA · nuclear cGAS restricts L1 retrotransposition by promoting TRIM41-mediated ORF2p ubiquitination; documents nuclear regulatory role for cGAS distinct from cytoplasmic sensor function ↩
doi:10.1016/j.ejmech.2020.113148 · Zhang G et al. · European Journal of Medicinal Chemistry · 2021 · in-vitro (colorectal cancer cells) · VCP/p97 inhibitors CB-5083, NMS-873; covalent inhibitor overcoming CB-5083 resistance; establishes pharmacological VCP inhibition tool compound landscape ↩
doi:10.3389/fragi.2025.1579813 · Jones KM et al. · Frontiers in Aging · 2025 · review · intersection of TREX1, cGAS, STING and the DNA damage theory of aging; LINE-1/retrotransposon-driven cGAS activation in aged cells ↩

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