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VASCULAR INFLAMMATION IN ATHEROSCLEROSIS: THE

MECHANISMS OF THE NLRP3 INFLAMMASOME IN THE GENESIS

OF ATHEROSCLEROTIC PLAQUE INSTABILITY

Luiz Coelho Soares Figueiredo1

Claudete Lúcia Carvalho Oliveira2

Arthur Valiatti Simões3

Mariana Manhães Pinto Braga4

Ana Luiza Latini Girolamy Daﬂ on5

Milene Vargas da Silva Batista6

Isabela da Silva Vieira7

Marcelo Costa Albani8

Gabriela Amaral Gonçalves9

Catarina Helena Costa Nunes Jório10

Valdinei Gonçalves dos Santos11

Bruno de Oliveira Figueiredo12

Gabriela Coelho Soares Figueiredo13

1 Campos School of Medicine (FMC), Campos dos Goytacazes, RJ, Brazil

2 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

3 Multivix University Center, Vitória, ES, Brazil

4 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

5 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

6 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

7 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

8 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

9 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

10 Centro Universitário Redentor (UniREDENTOR), Itaperuna, RJ, Brazil.

11 Universidade Brasil (UB), Fernandópolis, SP, Brazil

12 University of Vassouras, Vassouras, RJ, Brazil

13 UniFAMESC University Center, Bom Jesus do Itabapoana, RJ, Brazil

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Abstract: Introduction: Atherosclerosis is a chronic inﬂ ammatory disease characterized by lipid

accumulation and inﬂ ammatory cell inﬁ ltration within the arterial wall, representing the leading

cause of cardiovascular diseases worldwide. Recent evidence has demonstrated that the NLRP3

inﬂ ammasome plays a central role in the inﬂ ammatory response responsible for atherosclerosis

progression and atherosclerotic plaque instability. Objective: To analyze the mechanisms by which

the NLRP3 inﬂ ammasome contributes to vascular inﬂ ammation and the development of unstable

atherosclerotic plaques, as well as to discuss its potential as a therapeutic target. Methods: This

is a descriptive, exploratory, qualitative narrative literature review conducted using PubMed/

MEDLINE, Scopus, Web of Science, and the Virtual Health Library (VHL). Controlled descriptors

related to atherosclerosis, the NLRP3 inﬂ ammasome, and vascular inﬂ ammation were employed.

After applying the eligibility criteria, 20 studies were included in the qualitative analysis. Results

and discussion: The selected studies demonstrated that activation of the NLRP3 inﬂ ammasome by

cholesterol crystals, reactive oxygen species, and other danger signals promotes caspase-1 activation

and the release of IL-1β and IL-18, amplifying vascular inﬂ ammation. This process contributes to

foam cell formation, extracellular matrix degradation, ﬁ brous cap thinning, and plaque instability.

Furthermore, experimental and clinical evidence indicates that anti-inﬂ ammatory therapies targeting

the NLRP3 pathway reduce cardiovascular events, highlighting the translational potential of this

therapeutic strategy. Conclusion: The NLRP3 inﬂ ammasome is a key mediator of atherosclerosis

progression and plaque instability, representing both a promising biomarker and a potential therapeutic

target for preventing cardiovascular complications. Further studies are needed to optimize diagnostic

and therapeutic approaches aimed at modulating vascular inﬂ ammation.

Keywords: Atherosclerosis; Inﬂ ammation; NLRP3 Inﬂ ammasome.

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INTRODUCTION

Atherosclerosis is a chronic inﬂ ammatory disease of the arterial wall characterized by the

progressive accumulation of lipids, inﬂ ammatory cells, and ﬁ brous tissue in the vascular intima,

culminating in the formation of atherosclerotic plaques that can progress to luminal stenosis, rupture,

and thrombosis. It is the main pathophysiological basis of ischemic cardiovascular diseases, including

acute myocardial infarction and stroke, responsible for high morbidity and mortality worldwide. In

addition to the classic risk factors, such as dyslipidemia, hypertension, diabetes mellitus, and smoking,

recent studies show that immunoinﬂ ammatory mechanisms play a central role in both the initiation

and progression of atherosclerotic disease (HERRINGTON et al., 2016).

In recent decades, the NLRP3 (NOD-like receptor family pyrin domain containing 3)

inﬂ ammasome has emerged as one of the main regulators of the inﬂ ammatory response involved in

atherogenesis. This multiprotein complex is activated by several danger signals present in the vascular

microenvironment, including cholesterol crystals, reactive oxygen species, and products derived

from injured cells, promoting the activation of caspase-1 and the subsequent maturation of the pro-

inﬂ ammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18). The ampliﬁ cation of this

inﬂ ammatory cascade favors the recruitment of immune cells, intensiﬁ es endothelial dysfunction,

and perpetuates inﬂ ammation of the arterial wall (DUEWELL et al., 2010; GREBE; HOSS; LATZ,

2018).

Persistent activation of the NLRP3 inﬂ ammasome is closely related to the evolution of

atherosclerotic plaques to a vulnerable phenotype. The continuous production of inﬂ ammatory

mediators stimulates macrophage inﬁ ltration, foamy cell formation, extracellular matrix degradation

by metalloproteinases, and vascular smooth muscle cell apoptosis, culminating in the thinning of the

ﬁ brous cap and increased susceptibility to plaque rupture. These events are fundamental mechanisms

for the triggering of acute coronary syndromes, reinforcing the role of inﬂ ammation as a determining

element of atherosclerotic instability (BALDRIGHI; MALLAT; LI, 2017).

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At the same time, recent advances have directed efforts towards the development of therapeutic

strategies capable of selectively modulating the NLRP3 inﬂ ammasome and its inﬂ ammatory mediators.

The pharmacological inhibition of this pathway demonstrates potential to reduce the progression of

atherosclerosis and minimize cardiovascular events, consolidating the inﬂ ammasome as an important

therapeutic target in cardiovascular medicine. Although several molecular mechanisms have already

been described, there are still gaps regarding the integration between NLRP3 activation, vascular

inﬂ ammation, and the processes responsible for atherosclerotic plaque instability, justifying the

need for updated reviews on the subject (JABBOUR; KUMAR; HASSAN, 2023; KATSIMARDOS;

PAPAIOANNOU; KARAMITSOS, 2025).

In this context, the present study aims to analyze the mechanisms by which the NLRP3

inﬂ ammasome contributes to vascular inﬂ ammation and to the genesis of atherosclerotic plaque

instability. As speciﬁ c objectives, we seek to describe the main mechanisms of activation of the

NLRP3 inﬂ ammasome in atherosclerosis, to understand its interaction with the inﬂ ammatory pathways

involved in the progression of the disease and to discuss the therapeutic perspectives related to the

modulation of this molecular pathway. Thus, the following guiding question is established: how does

the activation of the NLRP3 inﬂ ammasome participate in vascular inﬂ ammation and contribute to

the development of atherosclerotic plaque instability, favoring the occurrence of acute cardiovascular

events?

MATERIAL AND METHODS

The present study consists of a narrative review of the literature, of a descriptive, exploratory

and qualitative nature, developed with the objective of gathering and analyzing the main scientiﬁ c

evidence about the role of the NLRP3 inﬂ ammasome in vascular inﬂ ammation and in the genesis of

atherosclerotic plaque instability.

The bibliographic search was carried out between June and July 2026, using the PubMed/

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MEDLINE, Scopus, Web of Science, and Virtual Health Library (VHL) databases, as they concentrate

high-impact journals in the area of biomedical and cardiovascular sciences. To elaborate the search

strategy, controlled descriptors from the Medical Subject Headings (MeSH) and Health Sciences

Descriptors (DeCS) vocabularies were used, combined by Boolean operators (AND and OR). The

main terms used were: “Atherosclerosis”, “NLRP3 Inﬂ ammasome”, “Vascular Inﬂ ammation”,

“Atherosclerotic Plaque”, “Plaque Instability”, “Inﬂ ammation”, “Interleukin-1 beta”, “Cholesterol

Crystals”, “Macrophages” and “Cardiovascular Diseases”, as well as their counterparts in Portuguese.

Original articles, systematic reviews, meta-analyses, clinical trials, experimental studies, and

narrative reviews published in Portuguese or English, between 2015 and 2026, available in full, and that

directly addressed the participation of the NLRP3 inﬂ ammasome in the inﬂ ammatory mechanisms

of atherosclerosis, in the progression of atherosclerotic plaque, or in therapeutic strategies related to

the modulation of this molecular pathway, were considered eligible. Duplicate studies, conference

abstracts, letters to the editor, editorials, book chapters, dissertations, theses, and papers that did not

have a direct relationship with the proposed theme were excluded.

The selection process of the studies was carried out in successive stages. Initially, the records

were identiﬁ ed in the databases and duplicates were removed. Next, the titles and abstracts were read

to assess the thematic relevance, and studies that did not meet the previously established eligibility

criteria were excluded. Potentially relevant articles were submitted to the full text reading, allowing

the conﬁ rmation of eligibility and the composition of the ﬁ nal review sample.

In the search process, 312 records were identiﬁ ed in the selected databases. After the removal

of 58 duplicate studies, 254 publications remained for screening by titles and abstracts. At this

stage, 186 articles were excluded because they were not directly related to the topic, addressed other

inﬂ ammatory diseases, did not investigate the NLRP3 inﬂ ammasome, or did not discuss mechanisms

of atherosclerotic plaque instability. Thus, 68 studies were submitted to reading in full. Of these, 48

publications were excluded because they did not meet the eligibility criteria, including unavailability

of the full text, exclusively experimental character with no applicability to the purpose of the review,

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absence of relevant data, or thematic overlap with more recent and robust studies. At the end of the

selection process, 20 articles made up the ﬁ nal sample of the review and supported the qualitative

analysis of the scientiﬁ c evidence. This process is illustrated in Figure 1 below.

Figure 1: Processing of the selected studies.

Source: authors, 2026

After selection, the included studies were submitted to a systematic process of information

extraction and organization. For each publication, the following were recorded: authors, year of

publication, country of origin, methodological design, study objective, population characteristics or

experimental model, main molecular mechanisms investigated, inﬂ ammatory biomarkers evaluated,

NLRP3 inﬂ ammasome activation pathways, main results and conclusions related to vascular

inﬂ ammation, atherosclerosis progression, and plaque instability.

The processing of the evidence occurred through qualitative and interpretative analysis, using

thematic analysis technique. Initially, the studies were grouped according to their axes of investigation,

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including: NLRP3 inﬂ ammasome activation mechanisms; participation of the IL-1β/IL-18 pathway

in the inﬂ ammatory response; role of cholesterol crystals and macrophages in atherogenesis; vascular

remodeling and atherosclerotic plaque instability; and therapeutic perspectives aimed at inhibiting

the inﬂ ammasome. Subsequently, a critical comparison of the ﬁ ndings was carried out, identifying

convergences, divergences and gaps in knowledge, allowing an integrated synthesis of the available

evidence.

As this is a research based exclusively on secondary data from published scientiﬁ c literature,

without direct involvement of human beings or use of identiﬁ able information, this study does not

require consideration by the Research Ethics Committee, according to the guidelines of Resolution

No. 510, of April 7, 2016, of the National Health Council.

RESULTS AND DISCUSSION

The analysis of the studies showed a consensus that atherosclerosis should be understood as

a chronic inﬂ ammatory disease, in which the innate immune response plays a determining role from

the formation of the fatty stretch mark to the rupture of the atherosclerotic plaque. In this context, the

NLRP3 inﬂ ammasome stands out as one of the main mediators of vascular inﬂ ammation, functioning

as an intracellular sensor capable of recognizing signs of damage and triggering the activation of

caspase-1, culminating in the release of the pro-inﬂ ammatory cytokines IL-1β and IL-18. This

process establishes a cycle of persistent inﬂ ammation that favors the progression of atherosclerotic

lesion and vascular remodeling (SWANSON; DENG; TING, 2019; LIBBY, 2022; KATSIMARDOS;

PAPAIOANNOU; KARAMITSOS, 2025).

Studies have shown that multiple stimuli participate in the activation of the NLRP3

inﬂ ammasome in the vascular environment. Cholesterol crystals, modiﬁ ed lipoproteins, reactive

oxygen species, cell necrosis products, and mitochondrial alterations promote oligomerization of

the inﬂ ammasomal complex, favoring an intense local inﬂ ammatory response. These mechanisms

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represent a link between lipid metabolism and innate immunity, explaining why lipid accumulation

alone is not sufﬁ cient to justify the evolution of atherosclerosis without the participation of inﬂ ammation

(KUBO; TAKAHASHI, 2020; LIAQAT et al., 2020; SWANSON; DENG; TING, 2019).

Another recurring aspect among the publications refers to the participation of macrophages in

the maintenance of vascular inﬂ ammation. After internalization of oxidized low-density lipoproteins

(LDL-ox), these cells differentiate into foamy cells and start producing inﬂ ammatory mediators that

perpetuate NLRP3 activation. At the same time, there is an increase in the expression of IL-1β, IL-18,

and other cytokines capable of amplifying leukocyte recruitment and stimulating new inﬂ ammatory

cells, favoring the expansion of atherosclerotic plaque and increasing its structural complexity

(TAKAHASHI, 2017; LIBBY, 2021; LIBBY; BORÉN; HANSSON, 2021).

The stability of atherosclerotic plaque depends on the balance between repairing and

inﬂ ammatory mechanisms. The studies analyzed demonstrate that persistent inﬂ ammasome

activation promotes extracellular matrix degradation through the induction of metalloproteinases,

apoptosis of vascular smooth muscle cells, and increase of the necrotic lipid nucleus. Consequently,

there is thinning of the ﬁ brous layer, reduction of the mechanical resistance of the plaque and greater

predisposition to rupture, an event directly related to the development of acute myocardial infarction

and ischemic stroke. These ﬁ ndings reinforce that the intensity of inﬂ ammation is a more relevant

factor for plaque vulnerability than the isolated degree of arterial stenosis (LIBBY, 2022; SIANOS;

KOUTROUBAKIS, 2023; KHAIR et al., 2024).

The systematic review conducted by Khair et al. (2024) consolidated evidence from

experimental and clinical studies demonstrating a consistent association between higher NLRP3

inﬂ ammasome activity and progression of atherosclerosis, corroborating observations previously

described by Takahashi (2017) and Kubo and Takahashi (2020). Taken together, these investigations

indicate that individuals with greater activation of this pathway have a greater intensity of the vascular

inﬂ ammatory response, greater formation of vulnerable plaques, and an increased risk of major

cardiovascular events.

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In recent years, the development of therapies targeting inﬂ ammation modulation has

signiﬁ cantly modiﬁ ed the understanding of atherosclerosis treatment. Ridker (2016) proposed a change

in the therapeutic paradigm by demonstrating that the selective reduction of inﬂ ammation, regardless

of lipid levels, could represent an effective strategy for cardiovascular prevention. This hypothesis

was later conﬁ rmed by the CANTOS study, in which IL-1β blockade by canakinumab signiﬁ cantly

reduced the incidence of recurrent cardiovascular events, consolidating the clinical importance of the

inﬂ ammatory pathway mediated by the NLRP3 inﬂ ammasome (RIDKER et al., 2017).

Similar results were observed with low-dose colchicine. The COLCOT clinical trial

demonstrated a signiﬁ cant reduction in cardiovascular events after acute myocardial infarction in

patients treated with colchicine, a drug that exerts an inhibitory effect on different components of

the inﬂ ammatory response, including the activation of the NLRP3 inﬂ ammasome. These ﬁ ndings

reinforce that pharmacological control of inﬂ ammation represents a complementary approach to

traditional lipid-lowering therapy, expanding the therapeutic possibilities for patients with established

atherosclerosis (TARDIF et al., 2019).

In addition to the direct inhibition of the inﬂ ammasome, new molecular strategies have been

investigated. Recent studies highlight the regulatory role of microRNAs, long non-coding RNAs, and

epigenetic mechanisms in modulating NLRP3 expression, opening perspectives for more speciﬁ c

therapies with a lower risk of systemic immunosuppression. Ryan, O’Neill, and Freeman (2024)

demonstrate that epigenetic modiﬁ cations directly inﬂ uence the intensity of the inﬂ ammatory response,

while Zhang et al. (2023) describe the therapeutic potential of non-coding RNAs as regulators of

inﬂ ammasome activation, conﬁ guring one of the main lines of translational research today.

Despite the advances obtained, important challenges persist for the clinical incorporation of

these strategies. The heterogeneity of the inﬂ ammatory response among individuals, the multiplicity

of pathways involved in NLRP3 activation, and the need for biomarkers capable of identifying patients

with greater therapeutic beneﬁ t still limit the routine application of these interventions. Recent

reviews highlight that the future of atherosclerosis treatment should involve personalized approaches,

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integrating inﬂ ammatory markers, genetic proﬁ ling, and molecular characteristics of atherosclerotic

plaque to target speciﬁ c therapies and increase clinical efﬁ cacy (SIANOS; KOUTROUBAKIS, 2023;

KATSIMARDOS; PAPAIOANNOU; KARAMITSOS, 2025).

Taken together, the analyzed evidence demonstrates that the NLRP3 inﬂ ammasome is one

of the main elements responsible for the connection between lipid metabolism, innate immunity

and vascular inﬂ ammation. Its participation in the activation of pro-inﬂ ammatory cytokines, cell

recruitment, vascular remodeling, and atherosclerotic plaque destabilization consolidates it as an

important biomarker and therapeutic target for the prevention of cardiovascular events. The integration

of knowledge from experimental studies, systematic reviews, and clinical trials indicates that the

therapeutic direction of this pathway represents one of the most promising prospects for translational

cardiology in the coming decades (LIBBY, 2021; LIBBY; BORÉN; HANSSON, 2021; KHAIR et al.,

2024; KATSIMARDOS; PAPAIOANNOU; KARAMITSOS, 2025).

FINAL CONSIDERATIONS

The present review showed that the NLRP3 inﬂ ammasome plays a central role in the

pathophysiology of atherosclerosis, acting as an important link between lipid metabolism, innate

immunity and vascular inﬂ ammation. The persistent activation of this complex promotes the production

of pro-inﬂ ammatory cytokines, intensiﬁ es the local immune response, and favors processes such as

the formation of foamy cells, degradation of the extracellular matrix, apoptosis of smooth muscle

cells, and thinning of the ﬁ brous cap, events that culminate in atherosclerotic plaque instability and

increase the risk of acute cardiovascular events.

The studies analyzed also demonstrated that the understanding of atherosclerosis goes

beyond the traditional concept of disease resulting exclusively from lipid accumulation, consolidating

inﬂ ammation as a determining component for both the progression and vulnerability of plaques. In

this scenario, the NLRP3 inﬂ ammasome pathway emerges as one of the main targets for innovative

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therapeutic interventions, supported by evidence from experimental studies, systematic reviews,

and clinical trials that demonstrate beneﬁ ts of modulation of the inﬂ ammatory response in reducing

cardiovascular events.

Although important advances have been achieved, challenges remain related to the

identiﬁ cation of biomarkers capable of selecting patients with greater inﬂ ammatory activity,

understanding the interactions between the different regulatory mechanisms of the inﬂ ammasome,

and developing more speciﬁ c, effective, and safe therapies. In addition, the inﬂ uence of genetic,

epigenetic, and non-coding RNA factors represents a promising ﬁ eld for future investigations.

Thus, it is concluded that the NLRP3 inﬂ ammasome is a fundamental component in the

genesis of atherosclerotic plaque instability, representing not only an important marker of vascular

inﬂ ammatory activity, but also a potential therapeutic target for the prevention of cardiovascular

complications. It is expected that new clinical and translational research will contribute to the

development of personalized treatment strategies, capable of integrating inﬂ ammation control

with conventional therapies, promoting better clinical outcomes and reducing the high burden of

atherosclerotic diseases in the population.

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