COVID-19 beyond the lungs: Unraveling its vascular impact and cardiovascular complications—mechanisms and therapeutic implications DOI Creative Commons
Ishita Saha, Oly Banerjee, Shampa Sarkar

и другие.

Science Progress, Год журнала: 2025, Номер 108(1)

Опубликована: Янв. 1, 2025

COVID-19, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), is primarily a illness but significantly affects the cardiovascular system as well. After entering body through tract, directly and indirectly disrupts vascular system. Vascular endothelial cells (ECs), which express ACE2 TMPRSS2, are targets for viral invasion. However, predominant cause of widespread damage “cytokine storm” induced immune response. This leads to EC activation, inflammation, neutrophil neutrophil–platelet aggregation, causing injury. Additionally, increased expression plasminogen activator inhibitor-1 balance between prothrombotic fibrinolytic processes, while activation renin–angiotensin–aldosterone adds oxidative stress endothelium. In heart, SARS-CoV-2 invades ECs, leading apoptosis pyroptosis, exacerbated inflammation elevated catecholamines. These factors contribute arrhythmias, strokes, myocardial infarction in cases COVID-19. narrative review aims explore mechanisms highlight resulting complications. It also identifies research gaps discusses potential therapeutic strategies mitigate impacts

Язык: Английский

COVID-19 in the Initiation and Progression of Atherosclerosis DOI Creative Commons
Vignesh Chidambaram,

Amudha Kumar,

Murrium I. Sadaf

и другие.

JACC Advances, Год журнала: 2024, Номер 3(8), С. 101107 - 101107

Опубликована: Июль 17, 2024

The incidence of atherosclerotic cardiovascular disease is increasing globally, especially in low- and middle-income countries, despite significant efforts to reduce traditional risk factors. Premature subclinical atherosclerosis has been documented association with several viral infections. magnitude the recent COVID-19 pandemic highlighted need understand between SARS-CoV-2 atherosclerosis. This review examines various pathophysiological mechanisms, including endothelial dysfunction, platelet activation, inflammatory immune hyperactivation triggered by infection, specific attention on their roles initiating promoting progression lesions. Additionally, it addresses pathogenic mechanisms which post-acute phase may contribute development vascular disease. Understanding overlap these syndromes enable novel therapeutic strategies. We further explore for guidelines closer follow-up often-overlooked evidence among patients COVID-19, particularly those cardiometabolic

Язык: Английский

Процитировано

10
Caspase-1 activation, IL-1/IL-6 signature and IFNγ-induced chemokines in lungs of COVID-19 patients DOI Creative Commons

Audrey Cambon,

Christophe Guervilly, Clémence Delteil

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 15

Опубликована: Янв. 15, 2025

COVID-19-associated acute-respiratory distress syndrome (C-ARDS) results from a direct viral injury associated with host excessive innate immune response mainly affecting the lungs. However, cytokine profile in lung compartment of C-ARDS patients has not been widely studied, nor compared to non-COVID related ARDS (NC-ARDS). To evaluate caspase-1 activation, IL-1 signature, and other inflammatory pathways tissue damage using post-mortem tissues, bronchoalveolar lavage fluids (BALF), serum across spectrum COVID-19 severity. Histological features were described activated-caspase-1 labeling was performed 40 biopsies. Inflammatory cytokines quantified BALF 19 steroid-treated-C-ARDSand NC-ARDS. Cytokine concentrations also measured 128 at different severity stages. Typical "diffuse alveolar damage" biopsies activated expression vascular lesions. Soluble Caspase-1p20, IL-1β, IL-1Ra, IL-6 lower level IFNγ CXCL-10, highly elevated steroid-treated-C-ARDS as well IL-1β appeared concentrated BALF, whereas circulating IL-1Ra comparable those correlated TNFα, TNFR1 CXCL8 however, significantly higher NC-ARDS C-ARDS, treated by steroid. In lungs both activation predominant IL-1β/IL-6 signature -associated chemokines are despite steroid treatment. These may be specifically targeted improve treatment limit damage.

Язык: Английский

Процитировано

1
Immunologic and inflammatory consequences of SARS-CoV-2 infection and its implications in renal disease DOI Creative Commons

Hiam Naiditch,

Michael R. Betts,

H. Benjamin Larman

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 15

Опубликована: Фев. 12, 2025

The emergence of the COVID-19 pandemic made it critical to understand immune and inflammatory responses SARS-CoV-2 virus. It became increasingly recognized that response was a key mediator illness severity its mechanisms needed be better understood. Early infection both tissue cells, such as macrophages, leading pyroptosis-mediated inflammasome production in an organ system for systemic oxygenation likely plays central role morbidity wrought by SARS-CoV-2. Delayed transcription Type I III interferons may lead early disinhibition viral replication. Cytokines interleukin-1 (IL-1), IL-6, IL-12, tumor necrosis factor α (TNFα), some which produced through involving nuclear kappa B (NF-κB), contribute hyperinflammatory state patients with severe COVID-19. Lymphopenia, more apparent among natural killer (NK) CD8+ T-cells, B-cells, can disease reflect direct cytopathic effects or end-organ sequestration. Direct activation endothelial cells mechanism systems are impacted. In this context, endovascular neutrophil extracellular trap (NET) formation microthrombi development seen lungs other organs throughout body, heart, gut, brain. kidney most impacted extrapulmonary owing high concentration ACE2 exposure kidney, acute tubular injury, myofibroblast activation, collapsing glomerulopathy select populations account COVID-19-related AKI CKD development. COVID-19-associated nephropathy (COVAN), particular, mediated IL-6 signal transducer activator 3 (STAT3) signaling, suggesting connection between chronic disease. Chronic manifestations also include conditions like Multisystem Inflammatory Syndrome Children (MIS-C) Adults (MIS-A) post-acute sequelae (PASC), spectrum clinical presentations persistent dysregulation. lessons learned those undergoing continued study have broad implications understanding infections’ immunologic consequences beyond coronaviruses.

Язык: Английский

Процитировано

1
NLRP3, the inflammasome and COVID-19 infection DOI Creative Commons
Maureen Yin, Laura Marrone, Christian G. Peace

и другие.

QJM, Год журнала: 2023, Номер 116(7), С. 502 - 507

Опубликована: Янв. 19, 2023

Abstract Severe coronavirus disease 2019 (COVID-19) is characterized by respiratory failure, shock or multiorgan dysfunction, often accompanied systemic hyperinflammation and dysregulated cytokine release. These features are linked to the intense rapid stimulation of innate immune response. The NACHT, LRR PYD domains-containing protein 3 (NLRP3) inflammasome a central player in inflammatory macrophage activation which via caspase-1 leads release mature forms proinflammatory cytokines interleukin (IL)-1β IL-18, cleavage Gasdermin D pyroptosis, an form cell death. Here, we discuss role NLRP3 COVID-19 clinical trials currently underway target treat severe COVID-19.

Язык: Английский

Процитировано

18
Targeting Inflammasome Activation in Viral Infection: A Therapeutic Solution? DOI Creative Commons

Chuan-Han Deng,

Tianqi Li,

Wei Zhang

и другие.

Viruses, Год журнала: 2023, Номер 15(7), С. 1451 - 1451

Опубликована: Июнь 27, 2023

Inflammasome activation is exclusively involved in sensing of innate immunity and inflammatory response during viral infection. Accumulating evidence suggests that the manipulation inflammasome assembly or its interaction with proteins are critical factors pathogenesis. Results from pilot clinical trials show encouraging results NLRP3 suppression reducing mortality morbidity SARS-CoV-2-infected patients. In this article, we summarize up-to-date understanding inflammasomes, including NLRP3, AIM2, NLRP1, NLRP6, NLRC4 various infections, particular focus on RNA viruses such as SARS-CoV-2, HIV, IAV, Zika virus DNA herpes simplex 1. We also discuss current achievement mechanisms infection-induced response, host defense, possible therapeutic solutions.

Язык: Английский

Процитировано

14
SARS-CoV-2 S1 subunit produces a protracted priming of the neuroinflammatory, physiological, and behavioral responses to a remote immune challenge: A role for corticosteroids DOI
Matthew G. Frank, Jayson B. Ball, Shelby Hopkins

и другие.

Brain Behavior and Immunity, Год журнала: 2024, Номер 121, С. 87 - 103

Опубликована: Июль 21, 2024

Язык: Английский

Процитировано

6
Recent progress and prospects for anti-cytokine therapy in preclinical and clinical acute lung injury DOI
Guilherme Pasetto Fadanni, João Β. Calixto

Cytokine & Growth Factor Reviews, Год журнала: 2023, Номер 71-72, С. 13 - 25

Опубликована: Июнь 1, 2023

Язык: Английский

Процитировано

12
Immunohematologic Biomarkers in COVID-19: Insights into Pathogenesis, Prognosis, and Prevention DOI Creative Commons
David R. Sweet, Michael L. Freeman, David A. Zidar

и другие.

Pathogens and Immunity, Год журнала: 2023, Номер 8(1)

Опубликована: Июнь 26, 2023

Coronavirus disease 2019 (COVID-19) has had profound effects on the health of individuals and healthcare systems worldwide. While workers frontlines have fought to quell multiple waves infection, efforts larger research community changed arch this pandemic as well. This review will focus biomarker discovery other identify features that predict outcomes, in so doing, possible effector passenger mechanisms adverse outcomes. Identifying measurable soluble factors, cell-types, clinical parameters a patient’s course legacy for study immunologic responses, especially stimuli, which induce an overactive, yet ineffectual immune system. As prognostic biomarkers were identified, some served represent pathways therapeutic interest trials. The conditions created urgency accelerated target identification validation. Collectively, these COVID-19 studies biomarkers, efficacy revealed responses stimuli are more heterogeneous than previously assumed. Understanding genetic acquired mediate divergent outcomes response global exposure is ongoing ultimately improve our preparedness future pandemics, well impact preventive approaches diseases.

Язык: Английский

Процитировано

11
Autism spectrum disorder and a possible role of anti-inflammatory treatments: experience in the pediatric allergy/immunology clinic DOI Creative Commons

Harumi Jyonouchi

Frontiers in Psychiatry, Год журнала: 2024, Номер 15

Опубликована: Июнь 24, 2024

Autism spectrum disorder (ASD 1 ) is a behaviorally defined syndrome encompassing markedly heterogeneous patient population. Many ASD subjects fail to respond the st line behavioral and pharmacological interventions, leaving parents seek out other treatment options. Evidence supports that neuroinflammation plays role in pathogenesis. However, underlying mechanisms likely vary for each patient, influenced by genetic, epigenetic, environmental factors. Although anti-inflammatory measures, mainly based on metabolic changes oxidative stress, have provided promising results some subjects, use of such measures requires careful selection clinical laboratory findings. Recent progress neuroscience molecular immunology has made it possible allow re-purposing currently available medications, used autoimmune chronic inflammatory conditions, as options subjects. On hand, emerging including biologic gate-keeper blockers, exert powerful effects specific mediators or signaling pathways. It will require both keen understanding action agents patients suitable treatment. This review attempt summarize already targeting patients, then applicable scientific rationale trial data, if available. In our experience, were treated under diagnoses autoimmune/autoinflammatory conditions and/or post-infectious neuroinflammation. there are little data specifically Therefore, these immunomodulating potential be discussed preclinical case reports, generated with medical conditions. hopefully highlight expanding scope treating

Язык: Английский

Процитировано

4
Monocyte/macrophage-mediated venous thrombus resolution DOI Creative Commons

Meng‐Jiao Lu,

Jiaqi Zhang,

Zhou-Yu Nie

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Июль 19, 2024

Venous thromboembolism (VTE) poses a notable risk of morbidity and mortality. The natural resolution the venous thrombus might be potential alternative treatment strategy for VTE. Monocytes/macrophages merge as pivotal cell types in gradual thrombus. In this review, vital role macrophages inducing inflammatory response, augmenting neovascularization, facilitating degradation fibrin collagen during was described. two phenotypes involved their dual functions were discussed. Macrophages expressing various factors, including cytokines receptors, adhesion molecules, chemokine vascular endothelial growth factor profibrinolytic- or antifibrinolytic-related enzymes, other elements, are explored to promote attenuate resolution. Furthermore, review provides comprehensive summary new promising therapeutic candidate drugs associated with monocytes/macrophages that have been demonstrated impair However, further clinical trials essential validate efficacy VTE therapy.

Язык: Английский

Процитировано

4