# Circadian Immunity and Vascular Inflammation in Cardiovascular Disease Chronotherapy Windows: Time for a Re-Assessment Researcher: Ge Zhang Chinese name: 张格 ORCID identity anchor: https://orcid.org/0000-0002-3116-3246 Canonical researcher: https://drgezhang.com/#person Journal: Med Research Year: 2026 Type: Article DOI: 10.1002/mdr2.70052 Canonical page: https://drgezhang.com/papers/doi-10-1002-mdr2-70052.html Markdown record: https://drgezhang.com/papers/doi-10-1002-mdr2-70052.md ## Full Authors 1. Tian Zhang 2. Ge Zhang 3. Tian-Ding Liu 4. Tianshu Gu 5. Fengyi Yu 6. Pengyuan Xu 7. Wunan Mi 8. Xuanjiang Zhao 9. Qian Guo 10. Honglin Zheng 11. Taiqi Zhao 12. Qiang Li 13. Di Lu 14. Mingxuan Duan 15. Chaoyang Yu 16. Ruhao Wu 17. Shiqian Zhang 18. Haonan Zhang 19. Zeyu Wang 20. Youyang Zheng 21. Yan Xiao 22. Zenglei Zhang 23. Ge Zhang ## Official Abstract Circadian rhythms orchestrate cardiovascular physiology by regulating immune and inflammatory pathways. Disruption of these rhythms profoundly alters vascular homeostasis, thereby promoting the onset and progression of cardiovascular diseases (CVD). Evidence from experimental and clinical studies demonstrates that circadian misalignment aggravates myocardial infarction, stroke, and hypertension by enhancing oxidative stress, dysregulating immune cell function, and activating inflammasomes. At the cellular level, macrophages and neutrophils exhibit rhythmic metabolic and inflammatory activities driven by circadian transcriptional networks such as the CLOCK‐BMAL1 complex, PER/CRY repressors, and secondary loops involving REV‐ERBα and RORγ. Epigenetic regulators including p300, THRAP3, and SRC‐2 further refine this temporal control of vascular inflammation. Disruption of these oscillatory systems increases NADPH oxidase activity, elevates reactive oxygen species (ROS) production, and activates NF‐κB signaling, leading to endothelial dysfunction and vascular injury. Given these temporal dynamics, chronotherapy, defined as the strategic timing of medication administration to synchronize with endogenous biological rhythms, emerges as a crucial determinant for cardiovascular therapeutic efficacy. Chronotherapeutic strategies, including pharmacological targeting of circadian regulators such as REV‐ERBα agonists, hold promise for mitigating vascular inflammation and improving cardiovascular outcomes. This review summarizes current evidence linking circadian rhythm disruption to immunoinflammatory mechanisms in cardiovascular disease and highlights novel avenues for time‐based therapeutic interventions. Text reproduced verbatim from Version of Record ([source](https://onlinelibrary.wiley.com/doi/full/10.1002/mdr2.70052)); [DOI](https://doi.org/10.1002/mdr2.70052); [CC-BY-4.0](https://creativecommons.org/licenses/by/4.0/). ## Research & review context ### Research fields - Cardiovascular chronobiology - Immune-vascular regulation ### Review topics - Circadian rhythms and vascular inflammation - Cardiovascular chronotherapy evidence and translation ### Scientific role Narrative synthesis connecting molecular clocks, immune regulation, vascular inflammation and cardiovascular treatment-timing research. ### Evidence position Narrative review of heterogeneous mechanistic, preclinical and clinical sources; not a systematic review, new experiment or universal medication-timing recommendation. ### Related concepts - Chronoimmunology - Treatment-timing evidence boundaries ### Possible citation contexts - Background: circadian organization of cardiovascular immune and inflammatory biology. - Evidence synthesis: distinctions between mechanistic chronotherapy rationale and unsettled clinical timing evidence. Possible literature-review contexts, not evidence of existing citations. Read the findings and Evidence Scope before citing the original article. ## Evidence Base **Circadian Immunity and Vascular Inflammation in Cardiovascular Disease Chronotherapy Windows: Time for a Re-Assessment** Narrative review of circadian immune-vascular mechanisms across cardiovascular disease, distinguishing preclinical chronotherapy rationale from heterogeneous and unresolved clinical timing evidence; no new data were created or analyzed. | Evidence | Value | | --- | --- | | Article type | Review Article | | Bibliography | 392 references | | Tables | 5 synthesis tables | | Figures | 9 figures | | New data | None created or analyzed | ### Counting note This is a narrative review. The 392 bibliography entries include heterogeneous evidence types and are not a systematic count of independent studies, experiments, animals or participants. Study-level denominators must not be summed into a synthetic n. The review reports no newly generated or newly analyzed dataset. ## Research Question How do circadian clock disruption and time-of-day biology interact with immune-cell trafficking, inflammatory signaling and vascular homeostasis across cardiovascular diseases, and what level of evidence supports translating these rhythms into cardiovascular chronotherapy? ## Author Evidence Summary This narrative review synthesizes experimental, mechanistic, epidemiological and clinical literature linking the circadian clock to cardiovascular immune and inflammatory biology. It organizes evidence around the CLOCK-BMAL1 transcriptional network, PER/CRY feedback, REV-ERB/ROR regulation, redox-sensitive signaling, NF-kB and NLRP3 inflammasome activity, cytokine and chemokine rhythms, and time-dependent immune-cell trafficking. These mechanisms are discussed across atherosclerosis, stroke, ischemic heart disease and heart failure. The review further evaluates preclinical chronotherapeutic strategies targeting clock and inflammatory pathways and contrasts them with a more limited and heterogeneous clinical evidence base. It does not report new experimental or clinical data, perform a meta-analysis, establish a universal cardiovascular dosing schedule, or demonstrate clinical efficacy for experimental clock-targeting compounds. ## Key Findings ### KF1: The review places CLOCK-BMAL1, PER/CRY and REV-ERB/ROR feedback loops at the center of temporal regulation of cardiovascular immune biology. Context: This is a synthesis of prior molecular and experimental literature rather than a new clock experiment. | Evidence | Value | | --- | --- | | Core clock machinery | BMAL1/ARNTL, CLOCK, PER1/2/3, CRY1/2, REV-ERB alpha/beta and ROR alpha/gamma are integrated with redox and epigenetic regulation. | Source locator: Sections 2.1-2.4; Figures 1-2; Tables 1-2. ### KF2: Circadian timing is synthesized as a regulator of PRR, NF-kB and NLRP3 inflammatory signaling and of cytokine, chemokine and adhesion-molecule rhythms. Context: These mechanisms derive from heterogeneous experimental systems and should not be represented as one fully demonstrated causal human pathway. | Evidence | Value | | --- | --- | | Inflammatory networks | The review discusses IL-1beta, IL-6, IL-18, TNF-alpha, CCL2, CXCL12, ICAM1, VCAM1 and related inflammatory networks. | Source locator: Sections 3-4; Figure 3; Table 3. ### KF3: The review describes circadian variation in immune-cell number, trafficking and function across neutrophils, monocytes/macrophages, lymphocytes and dendritic cells. Context: Timing, phase and mechanisms vary by species, tissue and experimental model. | Evidence | Value | | --- | --- | | Trafficking mechanisms | BMAL1, chemokine axes, sympathetic signaling and cell-intrinsic clocks are synthesized as contributors to rhythmic immune trafficking and function. | Source locator: Section 5; Figures 4-5. ### KF4: Circadian disruption is reviewed in relation to atherosclerosis, stroke, ischemic heart disease/myocardial infarction and heart failure through overlapping inflammatory, endothelial, metabolic and oxidative-stress mechanisms. Context: Evidence strength and causality differ materially across disease, mechanism and model. | Evidence | Value | | --- | --- | | Disease domains | The synthesis compares atherosclerosis, stroke, ischemic heart disease, myocardial infarction and heart failure rather than reporting one new cross-disease experiment. | Source locator: Sections 6.1-6.4; Figures 6-8. ### KF5: Preclinical studies provide a mechanistic rationale for time-dependent intervention targeting clock and inflammatory pathways. Context: This evidence is predominantly preclinical and must not be converted into human treatment-efficacy claims. | Evidence | Value | | --- | --- | | Preclinical strategies | The review discusses REV-ERB agonists, NLRP3 inhibitors, NF-kB pathway modulation, CCR2/CCL2 and CXCL12/CXCR4 strategies. | Source locator: Section 7.1; Table 4. ### KF6: Clinical chronotherapy evidence is heterogeneous and does not define a universal optimal dosing time for most cardiovascular drugs. Context: Physiological timing effects and mechanistic rationale are not equivalent to proven reductions in clinical outcomes. | Evidence | Value | | --- | --- | | Drug classes and timing | The review discusses aspirin, beta-blockers, melatonin, tPA, SGLT2 inhibitors, colchicine, ACEIs/ARBs, MRAs, ARNI and antihypertensive timing. | | Conflicting trials | Hygia and related studies reported bedtime-dosing benefits, whereas BedMed did not reproduce a cardiovascular-event benefit. | Source locator: Section 7.2; Table 5. ### KF7: The review identifies unresolved methodological and translational gaps that limit precision chronotherapy. Context: These gaps are part of the authors' discussion, not newly experimentally tested findings. | Evidence | Value | | --- | --- | | Research gaps | Constitutive-versus-inducible knockout-model differences, immune-cell-subpopulation heterogeneity, insufficient spatiotemporal resolution of vascular-immune interactions and the need for high-quality circadian-aware clinical trials are highlighted. | Source locator: Sections 8.1-8.4. ### KF8: Chronotherapy claims in this review require explicit separation of mechanistic rhythmicity, preclinical time-of-day efficacy, human surrogate effects and hard cardiovascular outcomes. Context: These evidence levels are not interchangeable. Human clinical timing evidence remains incomplete or conflicting for many cardiovascular therapies. | Evidence | Value | | --- | --- | | Human timing evidence | Bedtime aspirin can alter morning platelet reactivity, but cardiovascular event reduction has not been established by a large randomized trial; SGLT2-inhibitor and colchicine timing remain insufficiently tested. | | Outcome-level uncertainty | Antihypertensive bedtime-dosing studies have reported conflicting cardiovascular outcome results, including the Hygia and BedMed trials. | Source locator: Section 7.2; Table 5; Sections 8.1-8.4. ## Review Design & Evidence Synthesis ### Review profile - Study Design: Narrative evidence synthesis integrating molecular, cellular, animal, epidemiological and clinical chronotherapy literature. The article does not report a PRISMA-style systematic-search or study-selection workflow, quantitative meta-analysis, or a newly generated dataset. - Evidence Type: Narrative synthesis of heterogeneous preclinical, mechanistic, epidemiological and clinical evidence; no new dataset and no pooled meta-analytic effect estimate. - Diseases Covered: Atherosclerosis, Stroke, Ischemic heart disease, Myocardial infarction, Heart failure, Hypertension and blood-pressure chronotherapy where relevant - Translation Scope: Mechanistic rationale and preclinical chronotherapy are substantially stronger than the clinical evidence for universal time-specific dosing. - Evidence domains: Molecular circadian clock, Redox and epigenetic regulation, PRR / NF-kB / NLRP3 inflammatory signaling, Cytokine, chemokine and adhesion-molecule rhythmicity, Immune-cell trafficking and function, Cardiovascular disease mechanisms, Preclinical chronotherapy, Clinical chronotherapy and translation ## What This Review Adds - Provides an integrated immunovascular framework linking molecular circadian clocks to inflammatory signaling, leukocyte trafficking and cardiovascular disease biology. - Connects molecular mechanisms with disease-specific evidence across atherosclerosis, stroke, ischemic heart disease and heart failure. - Separates mechanistically attractive preclinical chronotherapy from the substantially less settled clinical evidence base. - Highlights why individualized circadian treatment strategies require stronger clinical validation rather than assuming a universal optimal dosing time. ## Evidence Scope ### Supports - Prior evidence links circadian clock networks with immune and vascular processes, inflammatory and redox pathways. - Immune-cell number, trafficking and functional state can vary with circadian timing across experimental contexts. - Experimental circadian disruption can alter cardiovascular inflammatory phenotypes, while cardiovascular physiology and events exhibit time-of-day patterns. - Preclinical evidence provides a mechanistic rationale for chronotherapy; some cardiovascular drugs show dosing-time-dependent physiological effects. - Clinical chronotherapy remains an active and unresolved translational field. ### Does Not Establish - A new patient cohort, new experimental data or a newly analyzed dataset. - A systematic review, meta-analysis or pooled quantitative effect size. - One universally causal circadian pathway across all cardiovascular diseases. - Human cardiovascular treatment efficacy of REV-ERB agonists or time-targeted NLRP3 or NF-kB inhibition. - Universal superiority of bedtime antihypertensive dosing or a dosing schedule suitable for every patient. - Reduced myocardial infarction or stroke outcomes from bedtime aspirin. - Established optimal dosing for SGLT2 inhibitors, colchicine, mineralocorticoid receptor antagonists or ARNI. - A guideline-level recommendation to change cardiovascular medication timing. ### Limitations - This is a narrative, non-systematic evidence synthesis with no new dataset or pooled effect estimate. - Species, tissues, disease models and evidence levels are heterogeneous; causal animal or cell findings cannot automatically be generalized to human cardiovascular disease. - Constitutive and inducible clock-gene knockout models may yield different findings. - Treatment-timing evidence is uneven across cardiovascular drug classes and many proposed chronotherapy windows remain theoretical or preclinical. - Clinical antihypertensive timing evidence is conflicting, including Hygia-versus-BedMed differences. - No universal dosing recommendation is established; high-quality circadian-aware randomized clinical trials are needed. ## Methodological & Translation Boundaries 1. This is a narrative evidence synthesis, not a systematic review or quantitative meta-analysis. 2. The 392 references are bibliography entries across heterogeneous evidence types, not a synthetic study count or sample size. 3. Mechanistic rhythmicity, animal chronopharmacology, human surrogate physiology and hard cardiovascular outcomes are different evidence levels. 4. Mouse Zeitgeber-time findings must not be converted directly into a human clock-time dosing prescription. 5. Changes in platelet activity, inflammatory biomarkers, blood pressure or other surrogate measures do not by themselves prove reductions in myocardial infarction, stroke or mortality. 6. Conflicting antihypertensive timing evidence remains conflicting; it does not support a universal bedtime-dosing recommendation. ## Chronotherapy Evidence Matrix | Intervention / drug class | Rhythmic biological rationale | Timing directly tested? | Evidence level | Main endpoint | Hard cardiovascular outcome status | Review locator | | --- | --- | --- | --- | --- | --- | --- | | REV-ERBα/β agonists — SR9009 / SR9011 | Circadian REV-ERB regulation of inflammatory signaling. | Yes, in selected preclinical models | Preclinical | NLRP3 / inflammatory signaling, MI/R injury, remodeling and cardiac function. | No human cardiovascular outcome validation; mouse ZT06 is not a human dosing recommendation. | Section 7.1.1; Table 4; reference 118. | | NLRP3 inhibitors — MCC950 and related compounds | Circadian variation in inflammatory and inflammasome signaling. | Limited / largely inferred from rhythmic biology | Preclinical | Inflammation, myocardial injury, atherosclerosis and remodeling in experimental models. | No established human cardiovascular chronotherapy outcome. | Section 7.1.2; Table 4. | | Aspirin | Circadian variation in morning platelet reactivity. | Yes | Human randomized crossover / physiological evidence | Morning platelet reactivity and related physiological measures. | Overall MI/stroke reduction from bedtime dosing remains unproven. | Section 7.2; Table 5; references 368-370. | | Beta-blockers | Daily variation in heart rate, blood pressure and autonomic activity. | Limited human evidence | Clinical / pharmacological | Heart rate, blood pressure and autonomic effects. | No universal outcome-based timing recommendation. | Section 7.2; Table 5. | | SGLT2 inhibitors | Rhythm-integrated dosing remains a proposed rather than validated clinical strategy. | No established rhythm-integrated clinical timing evidence | Clinical efficacy established independent of chronotherapy | Heart-failure and cardiorenal outcomes. | Chronotherapy-specific benefit unknown. | Section 7.2; Table 5. | | Colchicine | Rhythmic inflammation is a proposed timing rationale. | Not systematically evaluated | Clinical cardiovascular efficacy, but timing evidence lacking | Coronary disease / post-MI inflammatory risk. | Chronotherapy-specific outcome benefit unknown. | Section 7.2; Table 5. | | RAAS inhibitors / antihypertensive timing | Circadian variation in blood pressure. | Yes | Human randomized clinical evidence | Blood pressure and cardiovascular events. | Conflicting evidence; Hygia reported benefit whereas BedMed did not reproduce a cardiovascular-event benefit. | Section 7.2; Table 5; references 388-392. | | MRAs / ARNI | A chronotherapy-specific timing rationale remains unvalidated. | Insufficient or absent | Clinical efficacy established for their usual indications; chronotherapy evidence limited | Heart-failure / remodeling outcomes. | No established chronotherapy-specific outcome advantage. | Section 7.2; Table 5. | ## Selected Evidence Sources These are selected evidence sources used to verify claims on this author-controlled evidence page; they are not the complete reference list of the published review. 1. **SR9009 Administered for One Day After Myocardial Ischemia-Reperfusion Prevents Heart Failure in Mice by Targeting the Cardiac Inflammasome** — [https://doi.org/10.1038/s42003-019-0595-z](https://doi.org/10.1038/s42003-019-0595-z) Relationship: Direct preclinical evidence relevant to time-dependent REV-ERB agonist intervention after myocardial ischemia-reperfusion. Evidence: KF5, KF8 2. **Disruption of Circadian Rhythms by Shift Work Exacerbates Reperfusion Injury in Myocardial Infarction** — [https://doi.org/10.1016/j.jacc.2022.03.370](https://doi.org/10.1016/j.jacc.2022.03.370) Relationship: Translational human and experimental evidence linking shift-work-associated circadian disruption with myocardial infarction injury and prognosis. Evidence: KF4, KF8 3. **Time-Dependent Effects of Aspirin on Blood Pressure and Morning Platelet Reactivity: A Randomized Cross-Over Trial** — [https://doi.org/10.1161/hypertensionaha.114.04980](https://doi.org/10.1161/hypertensionaha.114.04980) Relationship: Human randomized crossover evidence for aspirin timing effects on physiological and platelet endpoints, not proof of reduced cardiovascular events. Evidence: KF6, KF8 4. **Effect of Aspirin Intake at Bedtime Versus on Awakening on Circadian Rhythm of Platelet Reactivity. A Randomised Cross-Over Trial** — [https://doi.org/10.1160/th-14-05-0453](https://doi.org/10.1160/th-14-05-0453) Relationship: Human randomized crossover evidence supporting timing-dependent platelet-reactivity effects. Evidence: KF6, KF8 5. **Bedtime Hypertension Treatment Improves Cardiovascular Risk Reduction: The Hygia Chronotherapy Trial** — [https://doi.org/10.1093/eurheartj/ehz754](https://doi.org/10.1093/eurheartj/ehz754) Relationship: Trial reporting cardiovascular benefit with bedtime antihypertensive dosing; retain the review's stated concerns regarding generalizability and conflicting subsequent evidence. Evidence: KF6, KF8 6. **Antihypertensive Medication Timing and Cardiovascular Events and Death: The BedMed Randomized Clinical Trial** — [https://doi.org/10.1001/jama.2025.4390](https://doi.org/10.1001/jama.2025.4390) Relationship: Randomized clinical evidence that did not reproduce the cardiovascular-event benefit reported by Hygia. Evidence: KF6, KF8 ## Q&A ### What type of article is this? It is a narrative Review Article synthesizing prior evidence. It reports no new experimental or clinical dataset, systematic study-selection workflow or pooled meta-analysis. Evidence: KF1, KF7 ### Which circadian clock components are central to cardiovascular immune regulation? The review centers on CLOCK-BMAL1, PER/CRY and REV-ERB/ROR feedback networks, including redox and epigenetic regulation; these are synthesized from prior work rather than tested as one new experiment. Evidence: KF1 ### How does circadian disruption interact with NF-kB and NLRP3? The review links clock and redox regulation with pattern-recognition receptor, NF-kB and NLRP3 inflammatory signaling, cytokines and chemokines. The underlying models are heterogeneous and do not establish one complete causal pathway in humans. Evidence: KF1, KF2 ### Which immune cells show circadian trafficking or functional rhythms? Prior evidence discussed for neutrophils, monocytes/macrophages, lymphocytes and dendritic cells indicates rhythmic numbers, trafficking or function, with phase and mechanism varying across species and tissues. Evidence: KF3 ### Which cardiovascular diseases are discussed? The review discusses atherosclerosis, stroke, ischemic heart disease and myocardial infarction, and heart failure, with hypertension considered in blood-pressure chronotherapy. Evidence strength differs across disease contexts. Evidence: KF4, KF6 ### Does the review prove that REV-ERB agonists treat cardiovascular disease in humans? No. REV-ERB agonist chronotherapy is discussed as mechanistic and preclinical rationale, not demonstrated human cardiovascular treatment efficacy. Evidence: KF5, KF8 ### Should all antihypertensive medications be taken at bedtime? No. Clinical evidence conflicts: Hygia and related studies reported bedtime-dosing benefits, while BedMed did not reproduce a cardiovascular-event benefit. The review does not support a universal bedtime recommendation. Evidence: KF6, KF8 ### Does bedtime aspirin have proven myocardial infarction or stroke outcome benefit? No large randomized trial cited by this review directly establishes reduced overall myocardial infarction or stroke incidence from bedtime aspirin dosing; physiological timing effects do not prove event reduction. Evidence: KF6, KF8 ### Are SGLT2-inhibitor, colchicine, MRA or ARNI dosing times clinically established? No. The review discusses these drug classes, but does not establish clinically validated optimal timing or universal cardiovascular outcome benefits for them. Evidence: KF6, KF8 ### Is this a systematic review or meta-analysis? No. The article reports no explicit systematic-search strategy, PRISMA study-selection workflow or quantitative meta-analysis; its 392 references are bibliography entries, not a systematic count of independent studies. Evidence: KF7 ### What gaps remain before cardiovascular chronotherapy can become precision medicine? Constitutive-versus-inducible model differences, immune-subpopulation and spatiotemporal heterogeneity, individualized rhythm variation and high-quality circadian-aware clinical trials remain important gaps. Evidence: KF7 ## Concepts & Entities ### Circadian Machinery BMAL1 / ARNTL, CLOCK, PER1, PER2, PER3, CRY1, CRY2, REV-ERBα / NR1D1, REV-ERBβ / NR1D2, RORα, RORγ ### Inflammatory And Redox Signaling NF-kB, NLRP3 inflammasome, NRF2, SIRT1, HIF-1alpha, pattern-recognition receptors, reactive oxygen species ### Cytokine And Trafficking Axes IL-1beta, IL-6, IL-18, TNF-alpha, CCL2-CCR2, CXCL12-CXCR4, ICAM1, VCAM1, CCR7, S1PR1, S1PR5 ### Cells neutrophils, monocytes, macrophages, lymphocytes, dendritic cells, endothelial cells, vascular smooth muscle cells ### Diseases atherosclerosis, stroke, ischemic heart disease, myocardial infarction, heart failure, hypertension ### Chronotherapy REV-ERB agonists, NLRP3 inhibitors, NF-kB pathway modulation, aspirin timing, beta-blockers, melatonin, tPA, SGLT2 inhibitors, colchicine, ACE inhibitors, ARBs, mineralocorticoid receptor antagonists, sacubitril/valsartan ## Related Research - [Molecular subtypes of ischemic heart disease based on circadian rhythm](https://drgezhang.com/papers/circadian-ihd.html) — Disease-specific computational analysis of circadian molecular heterogeneity in ischemic heart disease, complementing this review's broader mechanistic and chronotherapy synthesis. (DOI: 10.1038/s41598-024-65236-5) - [Smooth muscle cell fate decisions decipher a high-resolution heterogeneity within atherosclerosis molecular subtypes](https://drgezhang.com/papers/smc-fate.html) — Atherosclerotic vascular-cell-state evidence relevant to this review's discussion of vascular heterogeneity and inflammatory remodeling. (DOI: 10.1186/s12967-022-03795-9) - [The macrophage-derived motor protein KIF13B enhances MERTK-mediated efferocytosis and prevents atherosclerosis in mice](https://drgezhang.com/papers/doi-10-1093-eurheartj-ehaf523.html) — Experimental evidence for macrophage efferocytosis and inflammatory-resolution biology in atherosclerosis, complementary to this review's circadian immune-cell synthesis. (DOI: 10.1093/eurheartj/ehaf523) ## Publication & Provenance - DOI: https://doi.org/10.1002/mdr2.70052 - Doi: 10.1002/mdr2.70052 - Publisher: Wiley Online Library / Med Research - Publisher: https://doi.org/10.1002/mdr2.70052 - Article Type: Review Article - Access: Open Access - First Published: 05 January 2026 - Version Of Record: Med Research 2(2):236-279 - Formal Structure: Figures 1-9; Tables 1-5; references 1-392. - Data Availability: No new data were created or analyzed in this study. - Method Scope: Narrative synthesis; no explicit PRISMA systematic-search or study-selection workflow and no quantitative meta-analysis. ## Evidence-page notice This is an author-controlled evidence page for a narrative Review Article, not a new clinical study or treatment guideline. The publisher version remains the authoritative record. ## Links - DOI: https://doi.org/10.1002/mdr2.70052 - HTML page: https://drgezhang.com/papers/doi-10-1002-mdr2-70052.html - Google Scholar query: https://scholar.google.com/scholar?q=%22Circadian%20Immunity%20and%20Vascular%20Inflammation%20in%20Cardiovascular%20Disease%20Chronotherapy%20Windows%3A%20Time%20for%20a%20Re-Assessment%22 - ORCID: https://orcid.org/0000-0002-3116-3246