Adjacent Evidence Brief: Sulforaphane NRF2

Adjacent Evidence Brief: Sulforaphane NRF2

Abstract

This synthesis tests the thesis that evidence for Sulforaphane NRF2 is context-dependent, separating outcome-specific signals from broader claims and identifying the evidence gaps that should bound interpretation.

Evidence-honesty note: The retained evidence has no direct interventional hard-endpoint evidence; indirect, review-level, adjacent, or mechanistic sources are used only to bound interpretation. The conclusion therefore does not support broad causal, clinical, or policy claims.

This paper synthesizes evidence on Sulforaphane NRF2 across 21 included source papers and 902 high-confidence extracted claims.

The evidence profile contains no sources classified primarily as direct interventional hard-endpoint evidence, 16 adjacent clinical sources, and 5 mechanistic or model-system sources, with 5 cross-study disagreements across the evidence base.

Positive study-level signals are not the dominant direction in any outcome class; null signals are not the dominant direction in any outcome class; negative signals are not the dominant direction in any outcome class; mixed or heterogeneous signals are summarized in the contextual adjacent evidence, immune and inflammation, mechanism, and cardiometabolic outcome classes. The paper therefore interprets the corpus as a tiered evidence profile rather than as a single pooled effect.

The conclusion is that Sulforaphane NRF2 should be treated as a bounded geroscience hypothesis: the retained clinical and adjacent evidence profile defines the scope for targeted testing, while mixed and null findings limit any unqualified anti-aging claim.

Methods

Review type and protocol

This manuscript is reported as a Evidence brief. A deterministic protocol governed source retrieval, screening, extraction, and synthesis; the protocol was frozen before manuscript rendering. The full audit trail is in the supplementary methods_pack.json and the timestamped submission directory synthesis-sulforaphane_nrf2-v06-DAILY-2026-06-27T12-02-36Z.

Information sources

Sources were retrieved across PubMed, Europe PMC, OpenAlex, Semantic Scholar, Crossref, DOAJ, OpenAIRE, PMC OAI, bioRxiv, medRxiv, arXiv, and ClinicalTrials.gov. Retrieval window: 2026-06-27.

Search strategy

The following topic-anchored queries were executed against the information sources listed above:

• sulforaphane NRF2 AND aging AND human
• sulforaphane NRF2 AND older adults
• sulforaphane NRF2 AND randomized controlled trial
• sulforaphane AND aging AND human
• sulforaphane AND older adults
• sulforaphane AND randomized controlled trial
• NRF2 AND aging AND human
• NRF2 AND older adults
• NRF2 AND randomized controlled trial
• broccoli sprout AND aging AND human

Eligibility criteria

• Sources whose primary content addresses sulforaphane nrf2.
• Sources with extractable quantitative or qualitative findings.
• Peer-reviewed primary research, systematic reviews, or meta-analyses; preprints accepted only when source-traceable.
• Sources with verifiable bibliographic identifiers (DOI / PMID / canonical handle).

Selection of sources of evidence

The synthesis did not begin from an unfiltered database export. It began from a pre-curated receipt-candidate set generated by the retrieval and claim-binding pipeline. Of 161 records in the receipt-candidate union, 60 were classified as source candidates and 21 were admitted as traceable synthesis sources. Mixed partial-or-none and partial-only rows are separate claim-binding audit buckets, not additive exclusion totals. No additional records were excluded after final source admission.

source admission funnel

Admission bucket	n
Receipt candidate union	161
Classified source candidates	60
No extractable claims	36
None-only claim binding	7
Mixed partial-or-none claim-binding candidates	41
Partial-only claim-binding candidates	11
Strict high-confidence sources	6
Admitted final sources	21

Exclusion reasons

• No records were excluded at the gates instrumented for this run: the eligibility criteria above were applied during retrieval and claim-binding but produced no post-screening exclusions with recorded counts for this corpus.

Data items

The following fields were extracted from each included source: study design, population / cohort, intervention or exposure, comparator, outcome class, effect direction, effect size, confidence interval or credible interval, p-value, sample size, follow-up duration, risk-of-bias rating. Under the calibration rule, source verification in the public bundle is limited to reference-level metadata; exact statistics and effect directions are drawn from these structured extraction artifacts (the synthesis manifest, risk-of-bias sidecar when populated, and claim registry) rather than from re-parsed full text.

Risk-of-bias appraisal

Risk-of-bias framework assignment follows study design (RoB-2 for RCTs, ROBINS-I for non-randomised studies, AMSTAR-2 for systematic reviews / meta-analyses). Public appraisal claims are limited to populated risk_of_bias.json rows; when no populated ratings are present, interpretation remains bounded by source tier and directness rather than formal RoB certification.

Synthesis approach

Evidence-tension synthesis: claims grouped by outcome class (cardiometabolic, contextual adjacent evidence, immune and inflammation, mechanism); within-class agreement, disagreement, and directness gaps surfaced explicitly. Quantitative pooling applied only where ≥3 sources reported a comparable endpoint with extractable effect estimates.

AI-use disclosure

Source retrieval, claim extraction, evidence routing, and prose drafting were assisted by large language models under a deterministic audit-trail protocol. Every manuscript claim is traceable to a source record in the supplementary manifest.json. Final eligibility and interpretation decisions are author-verified.

Accountability

Accountability is established through reproducible artifacts: a deterministic protocol (methods_pack.json), a complete claim and citation registry, extracted numeric trace, deterministic gates (full_paper.journal_surface.json, pre_submit_gate.json, artifact_consistency.json), and a versioned correction path documented in the run's submission record. Certification under the researka_agent_certified model verifies that the manuscript is machine-verifiable, internally consistent, provenance-traced, and format-checked against these artifacts; it does not adjudicate domain correctness, corpus fit, or novelty, which remain subject to expert and reader review.

Results

Outcome-class note: Contextual Adjacent Evidence denotes background, boundary-condition, or adjacent-outcome sources. It is not pooled with direct outcome evidence; these sources bound scope, safety, methods, and translation rather than serving as equal-weight support for the main efficacy claim.

Evidence domain	Corpus slice	Strongest signal	Directness	Main limitation
Sulforaphane NRF2 / Contextual Adjacent Evidence	n=12; claims=441	significant source statistic in 8/12 sources; receipt-level direction coded unclear	11 indirect; 1 review	limited corpus depth in this outcome class
Sulforaphane NRF2 / Immune and Inflammation	n=4; claims=103	significant source statistic in 3/4 sources; receipt-level direction coded unclear	2 indirect; 2 mechanistic	limited corpus depth in this outcome class
Sulforaphane NRF2 / Mechanism	n=3; claims=160	significant source statistic in 3/3 sources; receipt-level direction coded unclear	3 mechanistic	limited corpus depth in this outcome class
Sulforaphane NRF2 / Cardiometabolic	n=2; claims=198	unclear signal in 1/2 sources	2 indirect	limited corpus depth in this outcome class

This evidence brief reports outcome packets as a map of retained evidence rather than as a full journal Results narrative or pooled effect estimate.

Contextual Adjacent Evidence Outcomes

In animal/preclinical evidence, contextual Adjacent Evidence remains a separate Results slice for Sulforaphane NRF2 (n=12; claims=441; significant source statistic in 8/12 sources; receipt-level direction coded unclear; 11 indirect; 1 review; limited corpus depth in this outcome class) and is not pooled into adjacent endpoint classes. Source-level findings are:

• Brown 2015 (Sulforaphane improves the bronchoprotective response in asthmatics through Nrf2-mediated gene pathways; representative statistic p = 0.01; source-level statistic reported; direction=mixed; directness=indirect; tier=B2).
• Bose 2020 (Sulforaphane prevents age‐associated cardiac and muscular dysfunction through Nrf2 signaling; representative statistic p = .0087; source-level statistic reported; direction=unclear; directness=indirect; tier=B2).
• Lu 2024 (Sulforaphane attenuates phosgene-induced acute lung injury via the Nrf2-HO-1/NQO1 pathway; representative statistic P<0.05; source-level statistic reported; direction=positive; directness=indirect; tier=B2).
• Padron 2022 (Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells; representative statistic p < 0.05; source-level statistic reported; direction=unclear; directness=indirect; tier=B2).

Direction reconciliation: receipt-level null or unclear coding is conservative claim-level coding. Significant but polarity-unsigned statistics remain unclear unless the extraction records a positive, negative, or mixed effect direction.

Immune and Inflammation Outcomes

Immune and Inflammation remains a separate Results slice for Sulforaphane NRF2 (n=4; claims=103; significant source statistic in 3/4 sources; receipt-level direction coded unclear; 2 indirect; 2 mechanistic; limited corpus depth in this outcome class) and is not pooled into adjacent endpoint classes. Source-level findings are:

• Subedi 2019 (Sulforaphane-Enriched Broccoli Sprouts Pretreated by Pulsed Electric Fields Reduces Neuroinflammation and Ameliorates; representative statistic P < 0.05; source-level statistic reported; direction=unclear; directness=mechanistic; tier=C1).
• Duran 2016 (A proof-of-concept clinical study examining the NRF2 activator sulforaphane against neutrophilic airway inflammation; representative statistic p = 0.001; source-level statistic reported; direction=unclear; directness=indirect; tier=B2).
• Chen 2025 (Effects of azithromycin on lung oxidative injury and immune function in mice infected with Mycoplasma pneumoniae based; representative statistic p < 0.05; source-level statistic reported; direction=null; directness=mechanistic; tier=C1).
• Ruhee 2025 (Effects of Sulforaphane Treatment on Skeletal Muscle from Exhaustive Exercise-Induced Inflammation and Oxidative Stress; 8 extracted claim(s); receipt-level direction is the coded finding; direction=null; directness=indirect; tier=B2).

Mechanism Outcomes

Mechanism remains a separate Results slice for Sulforaphane NRF2 (n=3; claims=160; significant source statistic in 3/3 sources; receipt-level direction coded unclear; 3 mechanistic; limited corpus depth in this outcome class) and is not pooled into adjacent endpoint classes. Source-level findings are:

• Ahmadian 2026 (Targeted activation of Nrf2 via sulforaphane-loaded exosomes attenuated azoospermic condition in the rat model; representative statistic p = 0.0009; source-level statistic reported; direction=unclear; directness=mechanistic; tier=C1).
• He 2022 (The Protective Effect of Sulforaphane on Dextran Sulfate Sodium-Induced Colitis Depends on Gut Microbial and; representative statistic P < 0.05; source-level statistic reported; direction=unclear; directness=mechanistic; tier=C1).
• Koduri 2026 (Oxidative Stress in Keratoconus Is Evident in Tear Fluid and Stromal Cells and Alleviated in Cell Culture by; representative statistic P ≤ 0.05; source-level statistic reported; direction=unclear; directness=mechanistic; tier=C1).

Cardiometabolic Outcomes

In animal/preclinical evidence, cardiometabolic remains a separate Results slice for Sulforaphane NRF2 (n=2; claims=198; unclear signal in 1/2 sources; 2 indirect; limited corpus depth in this outcome class) and is not pooled into adjacent endpoint classes. Source-level findings are:

• Sharma 2026 (The skeletal muscle slow myosin heavy chain regulates mammalian metabolic homeostasis through the NRF2 pathway; 155 extracted claim(s); receipt-level direction is the coded finding; direction=unclear; directness=indirect; tier=B2).
• Xin 2018 (Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ß/Fyn; 43 extracted claim(s); receipt-level direction is the coded finding; direction=null; directness=indirect; tier=B2).

Limitations

The principal limitation is evidence-role imbalance. The retained corpus contains no sources classified primarily as direct clinical evidence, 16 adjacent clinical sources, and 5 mechanistic or model-system sources, which means causal interpretation depends on how much weight is assigned to each evidence tier.

A second limitation is endpoint heterogeneity. Study-level signals span the contextual adjacent evidence outcome class, the contextual adjacent evidence, immune and inflammation, cardiometabolic outcome classes, no dominant outcome class, and the contextual adjacent evidence outcome class; these domains cannot be pooled narratively without losing clinically relevant differences in measurement, population, and study design.

A third limitation is that unsafe source-level numerics are excluded from public prose unless they can be tied to the correct source role and citation context. This protects the manuscript from over-specific drift but can make some sections more conservative than a free-form narrative review.

Conclusion

For Sulforaphane NRF2, the final interpretation is deliberately tiered: the retained clinical and adjacent evidence profile defines a bounded geroscience rationale, but the corpus does not support treating mechanistic target engagement, intermediate biomarkers, and patient-relevant outcomes as interchangeable evidence. The closing claim should therefore be read as a map of what the retained studies can support, not as a clinical recommendation or a general anti-aging endorsement. Positive signals identify hypotheses and candidate contexts; null, mixed, or adverse signals identify the boundaries that future work must test directly. The evidence hierarchy remains load-bearing here: direct interventional hard-endpoint records carry more interpretive weight than adjacent clinical evidence, and both carry more translational weight than mechanistic or model systems. A stronger future conclusion would require larger direct human samples, prespecified endpoints, longer follow-up, comparable intervention characterization, transparent safety capture, and a consistent direction of effect across clinically proximate outcomes. Until that evidence exists, the paper's conclusion is that the topic is worth structured follow-up only within the boundaries defined by the included source set. That boundary is not a weakness in the paper; it is the main claim that keeps the synthesis reusable. Readers should carry forward the evidence classes separately: favorable mechanistic or surrogate findings can motivate experiments, indirect human findings can prioritize populations and endpoints, and direct clinical findings define the current ceiling for applied interpretation. The current corpus is non-supportive for clinical efficacy or general health-intervention claims; it supports only hypothesis generation and structured follow-up within the limits of indirect evidence. Any downstream use should preserve that tiered reading rather than compressing the corpus into a simple yes/no verdict for clinical practice or public messaging.

What This Synthesis Adds

This synthesis maps 21 included sources on Sulforaphane Nrf2 across 4 outcome classes and 5 cross-study disagreements. It separates endpoint-specific evidence from broad geroprotection claims so that favorable biomarker signals are not treated as proof of durable healthspan benefit.

Across 21 curated reference papers, the evidence base for Sulforaphane Nrf2 shows a context-dependent profile. Positive signals appear in: contextual other. Null findings dominate: contextual other, immune inflammation. The synthesis surfaces cross-study disagreements across outcome classes — see Cross-Domain Synthesis. The Sulforaphane Nrf2 anti-aging case as currently constituted is incomplete: mechanistic plausibility coexists with mixed or sparse human-RCT evidence, and the boundary conditions remain to be established.

In animal/preclinical evidence, the strongest unresolved contrast is the null vs positive between Lu 2024 and Xie 2025 on contextual adjacent evidence (severity 4/5), which defines the boundary condition future studies must test rather than smooth over.

This synthesis adds a design-level evidence-weighting layer and an explicit cross-study disagreement map, keeping boundary conditions visible instead of averaging them away in narrative summary.

Boundary-Condition Matrix

Evidence domain	Direct sources	Indirect / mechanism sources	Direction profile	Interpretation boundary
cardiometabolic	0	2	null, unclear	direct interventional hard-endpoint gap
contextual adjacent evidence	0	12	mixed, null, positive, unclear	conflict-resolution gap
mechanism	0	3	unclear	direct interventional hard-endpoint gap
immune and inflammation	0	4	null, unclear	direct interventional hard-endpoint gap

Evidence-Gap Priority

Priority	Gap	Rationale
P1	cardiometabolic: direct interventional hard-endpoint gap	0 direct and 2 indirect sources; direction profile: null, unclear
P2	contextual adjacent evidence: conflict-resolution gap	0 direct and 12 indirect sources; direction profile: mixed, null, positive, unclear
P3	mechanism: direct interventional hard-endpoint gap	0 direct and 3 indirect sources; direction profile: unclear
P4	immune and inflammation: direct interventional hard-endpoint gap	0 direct and 4 indirect sources; direction profile: null, unclear

Next-Study Design Recommendation

The next high-yield study for Sulforaphane Nrf2 should target the cardiometabolic evidence gap, pre-register the primary endpoint, separate clinical from mechanistic endpoints, preserve safety and adherence capture, and include an analysis plan that can falsify the current boundary-condition claim rather than only confirming a favorable direction. Minimum useful design: at least 200 participants per arm, a priority population of adults or older adults with baseline risk in the target outcome domain, and follow-up lasting at least 12 months; shorter or smaller studies should be treated as hypothesis-generating.

Evidence Snapshot

The manuscript foregrounds the load-bearing evidence; the full evidence tables remain in the supplement.

Load-Bearing Included Studies

• In animal/preclinical evidence, Sharma 2026; tier=B2; directness=indirect; endpoint=cardiometabolic; direction=unclear.
• Brown 2015; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=mixed; representative statistic=P = 0.0005.
• Bose 2020; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=unclear; representative statistic=P < 0.0001.
• Clifford 2021; tier=B2; directness=review; endpoint=contextual adjacent evidence; direction=null.
• Lu 2024; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=positive; representative statistic=P < 0.001.
• Xin 2018; tier=B2; directness=indirect; endpoint=cardiometabolic; direction=null.
• Padron 2022; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=unclear; representative statistic=P < 0.01.
• Fu 2026; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=null; representative statistic=P = 0.517.
• Duran 2016; tier=B2; directness=indirect; endpoint=immune inflammation; direction=unclear; representative statistic=P = 0.001.
• Doss 2016; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=unclear; representative statistic=P = 0.0082.

Source Classification Map

Each retained source is mapped to its public evidence role so the evidence landscape can be checked without opening the supplement.

• In animal/preclinical evidence, Sharma 2026: outcome=cardiometabolic; directness=indirect; tier=B2; direction=unclear; claims=155.
• Brown 2015: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=mixed; claims=142.
• Bose 2020: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=80.
• Clifford 2021: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=null; claims=46.
• Lu 2024: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=positive; claims=45.
• Xin 2018: outcome=cardiometabolic; directness=indirect; tier=B2; direction=null; claims=43.
• Padron 2022: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=36.
• Fu 2026: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=31.
• Duran 2016: outcome=immune inflammation; directness=indirect; tier=B2; direction=unclear; claims=27.
• Doss 2016: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=19.
• Wise 2016: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=14.
• Mohammad 2022: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=13.
• Ruhee 2025: outcome=immune inflammation; directness=indirect; tier=B2; direction=null; claims=8.
• OMealey 2016: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=6.
• Xie 2025: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=5.
• Mitra 2026: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=4.
• Ahmadian 2026: outcome=mechanism; directness=mechanistic; tier=C1; direction=unclear; claims=70.
• He 2022: outcome=mechanism; directness=mechanistic; tier=C1; direction=unclear; claims=61.
• Subedi 2019: outcome=immune inflammation; directness=mechanistic; tier=C1; direction=unclear; claims=46.
• Koduri 2026: outcome=mechanism; directness=mechanistic; tier=C1; direction=unclear; claims=29.
• Chen 2025: outcome=immune inflammation; directness=mechanistic; tier=C1; direction=null; claims=22.

Classification Criteria

• Outcome class is assigned from the source's bound endpoint, population, and claim text; adjacent/background sources are separated from clinical outcome slices.
• Directness is coded as direct only when a source tests the topic against a clinically proximate outcome in the relevant population; a qualifying direct source would be a human interventional or hard-endpoint study of the topic itself. Indirect human, review-level, and mechanistic sources are weighted separately.
• Directional signal is counted within the assigned outcome class only. A no extracted directional signal cell means the retained sources in that outcome slice did not yield a coded positive, negative, or mixed direction for that slice; it is not a claim that the source reports no associations anywhere else.
• Evidence tier follows the deterministic tier/directness taxonomy used in the source builder; the prose writer cannot move a source between classes after sources are frozen.

Load-Bearing Tensions

• Additional corpus sources included animal/preclinical evidence; severity 4 null vs positive: Lu 2024 vs Xie 2025; Lu 2024 (positive on contextual other) vs Xie 2025 (null on contextual other) — partial conflict
• Severity 4 null vs positive: Lu 2024 vs Fu 2026; Lu 2024 (positive on contextual other) vs Fu 2026 (null on contextual other) — partial conflict
• Severity 4 null vs positive: Lu 2024 vs Wise 2016; Lu 2024 (positive on contextual other) vs Wise 2016 (null on contextual other) — partial conflict
• Severity 4 null vs positive: Lu 2024 vs OMealey 2016; Lu 2024 (positive on contextual other) vs OMealey 2016 (null on contextual other) — partial conflict
• Severity 4 null vs positive: Lu 2024 vs Clifford 2021; Lu 2024 (positive on contextual other) vs Clifford 2021 (null on contextual other) — partial conflict

References

• Sharma 2026. The skeletal muscle slow myosin heavy chain regulates mammalian metabolic homeostasis through the NRF2 pathway. Science Advances, 2026. DOI: 10.1126/sciadv.aed2478. PMID: 42234761.
• Brown 2015. Sulforaphane improves the bronchoprotective response in asthmatics through Nrf2-mediated gene pathways. Respiratory Research, 2015. DOI: 10.1186/s12931-015-0253-z. PMID: 26369337.
• Bose 2020. Sulforaphane prevents age‐associated cardiac and muscular dysfunction through Nrf2 signaling. Aging Cell, 2020. DOI: 10.1111/acel.13261. PMID: 33067900.
• Ahmadian 2026. Targeted activation of Nrf2 via sulforaphane-loaded exosomes attenuated azoospermic condition in the rat model. Scientific Reports, 2026. DOI: 10.1038/s41598-026-40709-x. PMID: 41708791.
• He 2022. The Protective Effect of Sulforaphane on Dextran Sulfate Sodium-Induced Colitis Depends on Gut Microbial and Nrf2-Related Mechanism. Frontiers in Nutrition, 2022. DOI: 10.3389/fnut.2022.893344. PMID: 35832050.
• Subedi 2019. Sulforaphane-Enriched Broccoli Sprouts Pretreated by Pulsed Electric Fields Reduces Neuroinflammation and Ameliorates Scopolamine-Induced Amnesia in Mouse Brain through Its Antioxidant Ability via Nrf2-HO-1 Activation. Oxidative Medicine and Cellular Longevity, 2019. DOI: 10.1155/2019/3549274. PMID: 31049133.
• Clifford 2021. The effect of dietary phytochemicals on nuclear factor erythroid 2-related factor 2 (Nrf2) activation: a systematic review of human intervention trials. Molecular Biology Reports, 2021. DOI: 10.1007/s11033-020-06041-x. PMID: 33515348.
• Lu 2024. Sulforaphane attenuates phosgene-induced acute lung injury via the Nrf2-HO-1/NQO1 pathway. Journal of Thoracic Disease, 2024. DOI: 10.21037/jtd-24-819. PMID: 39552873.
• Xin 2018. Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ß/Fyn pathway. Redox Biology, 2018. DOI: 10.1016/j.redox.2017.12.016. PMID: 29353218.
• Padron 2022. Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells. Biomolecules, 2022. DOI: 10.3390/biom12060766. PMID: 35740891.
• Fu 2026. Sulforaphane Alleviates Zearalenone-Induced Oxidative Stress in Bovine Mammary Epithelial Cells. Animals : an Open Access Journal from MDPI, 2026. DOI: 10.3390/ani16111602. PMID: 42278036.
• Koduri 2026. Oxidative Stress in Keratoconus Is Evident in Tear Fluid and Stromal Cells and Alleviated in Cell Culture by Sulforaphane. Investigative Ophthalmology & Visual Science, 2026. DOI: 10.1167/iovs.67.5.1. PMID: 42065481.
• Duran 2016. A proof-of-concept clinical study examining the NRF2 activator sulforaphane against neutrophilic airway inflammation. Respiratory Research, 2016. DOI: 10.1186/s12931-016-0406-8. PMID: 27450419.
• Chen 2025. Effects of azithromycin on lung oxidative injury and immune function in mice infected with Mycoplasma pneumoniae based on the Nrf2/ARE signaling pathway. Central-European Journal of Immunology, 2025. DOI: 10.5114/ceji.2025.152018. PMID: 41438358.
• Doss 2016. Phase 1 Study of a Sulforaphane-Containing Broccoli Sprout Homogenate for Sickle Cell Disease. PLoS ONE, 2016. DOI: 10.1371/journal.pone.0152895. PMID: 27071063.
• Wise 2016. Lack of Effect of Oral Sulforaphane Administration on Nrf2 Expression in COPD: A Randomized, Double-Blind, Placebo Controlled Trial. PLoS ONE, 2016. DOI: 10.1371/journal.pone.0163716. PMID: 27832073.
• Mohammad 2022. Age-Related Mitochondrial Impairment and Renal Injury Is Ameliorated by Sulforaphane via Activation of Transcription Factor NRF2. Antioxidants, 2022. DOI: 10.3390/antiox11010156. PMID: 35052660.
• Ruhee 2025. Effects of Sulforaphane Treatment on Skeletal Muscle from Exhaustive Exercise-Induced Inflammation and Oxidative Stress Through the Nrf2/HO-1 Signaling Pathway. Antioxidants, 2025. DOI: 10.3390/antiox14020210. PMID: 40002396.
• OMealey 2016. Sulforaphane is a Nrf2-independent inhibitor of mitochondrial fission. Redox Biology, 2016. DOI: 10.1016/j.redox.2016.11.007. PMID: 27889639.
• Xie 2025. Sulforaphane alleviates hepatocyte pyroptosis via activating Nrf2-HO-1 signaling during septic acute liver injury. Frontiers in Pharmacology, 2025. DOI: 10.3389/fphar.2025.1690067. PMID: 41181585.
• Mitra 2026. Effect of Glucoraphanin on the Abundance of Nrf2 Regulated Genes Within Circulating Small Extracellular Vesicles: A Pilot Dietary Intervention. Molecular Nutrition & Food Research, 2026. DOI: 10.1002/mnfr.70397. PMID: 41603376.

Background References

Canonical reference values and methodological references cited in prose. Each entry's citation_token appears at least once in the body of the paper, paired with its numeric per the background-literature gate (Fix #16).