Role of Pyroptosis in Cardiovascular Diseases and its Therapeutic Implications
Pyroptotic cell death or pyroptosis is characterized by caspase-1-dependent formation of plasma membrane pores, leading to the release of pro-inflammatory cytokines and cell lysis. Pyroptosis tightly controls the inflammatory responses and coordinates antimicrobial host defenses by releasing pro-inf...
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| Vydané v: | International journal of biological sciences Ročník 15; číslo 7; s. 1345 - 1357 |
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| Hlavní autori: | , , |
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| Jazyk: | English |
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| Abstract | Pyroptotic cell death or pyroptosis is characterized by caspase-1-dependent formation of plasma membrane pores, leading to the release of pro-inflammatory cytokines and cell lysis. Pyroptosis tightly controls the inflammatory responses and coordinates antimicrobial host defenses by releasing pro-inflammatory cellular contents, such as interleukin (IL)-1β and IL-18, and consequently expands or sustains inflammation. It is recognized as an important innate immune effector mechanism against intracellular pathogens. The induction of pyroptosis is closely associated with the activation of the NOD-like receptor 3 (NLRP3) inflammasome which has been linked to key cardiovascular risk factors including hyperlipidemia, diabetes, hypertension, obesity, and hyperhomocysteinemia. Emerging evidence has indicated pyroptosis as an important trigger and endogenous regulator of cardiovascular inflammation. Thus, pyroptosis may play an important role in the pathogenesis of cardiovascular diseases. Design of therapeutic strategies targeting the activation of NLRP3 inflammasome and pyroptosis holds promise for the treatment of cardiovascular diseases. |
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| AbstractList | Pyroptotic cell death or pyroptosis is characterized by caspase-1-dependent formation of plasma membrane pores, leading to the release of pro-inflammatory cytokines and cell lysis. Pyroptosis tightly controls the inflammatory responses and coordinates antimicrobial host defenses by releasing pro-inflammatory cellular contents, such as interleukin (IL)-1β and IL-18, and consequently expands or sustains inflammation. It is recognized as an important innate immune effector mechanism against intracellular pathogens. The induction of pyroptosis is closely associated with the activation of the NOD-like receptor 3 (NLRP3) inflammasome which has been linked to key cardiovascular risk factors including hyperlipidemia, diabetes, hypertension, obesity, and hyperhomocysteinemia. Emerging evidence has indicated pyroptosis as an important trigger and endogenous regulator of cardiovascular inflammation. Thus, pyroptosis may play an important role in the pathogenesis of cardiovascular diseases. Design of therapeutic strategies targeting the activation of NLRP3 inflammasome and pyroptosis holds promise for the treatment of cardiovascular diseases. Pyroptotic cell death or pyroptosis is characterized by caspase-1-dependent formation of plasma membrane pores, leading to the release of pro-inflammatory cytokines and cell lysis. Pyroptosis tightly controls the inflammatory responses and coordinates antimicrobial host defenses by releasing pro-inflammatory cellular contents, such as interleukin (IL)-1β and IL-18, and consequently expands or sustains inflammation. It is recognized as an important innate immune effector mechanism against intracellular pathogens. The induction of pyroptosis is closely associated with the activation of the NOD-like receptor 3 (NLRP3) inflammasome which has been linked to key cardiovascular risk factors including hyperlipidemia, diabetes, hypertension, obesity, and hyperhomocysteinemia. Emerging evidence has indicated pyroptosis as an important trigger and endogenous regulator of cardiovascular inflammation. Thus, pyroptosis may play an important role in the pathogenesis of cardiovascular diseases. Design of therapeutic strategies targeting the activation of NLRP3 inflammasome and pyroptosis holds promise for the treatment of cardiovascular diseases.Pyroptotic cell death or pyroptosis is characterized by caspase-1-dependent formation of plasma membrane pores, leading to the release of pro-inflammatory cytokines and cell lysis. Pyroptosis tightly controls the inflammatory responses and coordinates antimicrobial host defenses by releasing pro-inflammatory cellular contents, such as interleukin (IL)-1β and IL-18, and consequently expands or sustains inflammation. It is recognized as an important innate immune effector mechanism against intracellular pathogens. The induction of pyroptosis is closely associated with the activation of the NOD-like receptor 3 (NLRP3) inflammasome which has been linked to key cardiovascular risk factors including hyperlipidemia, diabetes, hypertension, obesity, and hyperhomocysteinemia. Emerging evidence has indicated pyroptosis as an important trigger and endogenous regulator of cardiovascular inflammation. Thus, pyroptosis may play an important role in the pathogenesis of cardiovascular diseases. Design of therapeutic strategies targeting the activation of NLRP3 inflammasome and pyroptosis holds promise for the treatment of cardiovascular diseases. |
| Author | Wang, Renqing Zeng, Cheng Tan, Hongmei |
| AuthorAffiliation | 1 Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China 2 Department of pathology, the Affiliated Drum Tower Hospital of Medical School of Nanjing University, Nanjing 21008, China |
| AuthorAffiliation_xml | – name: 2 Department of pathology, the Affiliated Drum Tower Hospital of Medical School of Nanjing University, Nanjing 21008, China – name: 1 Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China |
| Author_xml | – sequence: 1 givenname: Cheng surname: Zeng fullname: Zeng, Cheng – sequence: 2 givenname: Renqing surname: Wang fullname: Wang, Renqing – sequence: 3 givenname: Hongmei surname: Tan fullname: Tan, Hongmei |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31337966$$D View this record in MEDLINE/PubMed |
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| Keywords | pyroptosis NLRP3 cardiovascular diseases inflammation caspase-1 inflammasome |
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| SubjectTerms | Activation Animals Autophagy Cardiovascular diseases Cardiovascular Diseases - metabolism Cardiovascular Diseases - therapy Carrier Proteins - metabolism Caspase Caspase 1 - metabolism Caspase-1 Cell death Cytokines Diabetes mellitus Diabetic Cardiomyopathies - metabolism Health risks Heart Failure - metabolism Humans Hyperhomocysteinemia Hyperlipidemia Hypertension Inflammasomes Inflammasomes - metabolism Inflammation Interleukin 18 Interleukins - metabolism Lysis Macrophages - metabolism Myocarditis - metabolism Myocarditis - virology NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Pathogenesis Pyroptosis Review Risk analysis Risk Factors |
| Title | Role of Pyroptosis in Cardiovascular Diseases and its Therapeutic Implications |
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