Inflammasomes in cardiovascular diseases.

نویسنده

  • Nisha Jain Garg
چکیده

NOD-like receptors (NLRs) constitute a recently identified family of macromolecules that participate in regulation of innate immune responses. To date, 23 members of the NLR family are identified in humans. Diverse NLRs are stimulated by a broad range of pathogen- or danger-associated molecular patterns, and collectively function as intracellular pattern recognition receptors (PRRs). The most studied inflammasomes are NLRP1 and NLRP3 that process inactive pro-caspase-1 to its active form, allowing the cleavage and subsequent activation of pro-IL-1β and pro-IL-18, and initiation of inflammatory responses. Three models, based upon extracellular ATP/K(+) flux, lysosomal release of cathepsin, and reactive oxygen species, have been proposed to be involved in signaling activation of NLRs and downstream events. In this review, I discuss the current state of knowledge related to the roles of NLRs and inflammasomes in the development of cardiovascular diseases.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Cardiovascular pathobiology of inflammasomes: inflammatory machinery and beyond.

SIGNIFICANCE In response to infection or cellular stress, inflammasomes are assembled and activated to mediate host defense and to initiate or promote the development of different diseases, in particular, autoinflammatory diseases and chronic degenerative diseases. Understanding of inflammasomes and related physiological and pathological relevance to the cardiovascular system will open a new ch...

متن کامل

Inflammasomes in neuroinflammation and changes in brain function: a focused review

Recent literature has pointed to the existence of inflammasome-mediated inflammatory pathways in central nervous system (CNS) disorders and associated changes in behavior. Neuroinflammation, which is an innate immune response in the CNS against harmful and irritable stimuli such as pathogens and metabolic toxic waste, as well as to chronic mild stress, is mediated by protein complexes known as ...

متن کامل

The cardiac glycoside ouabain activates NLRP3 inflammasomes and promotes cardiac inflammation and dysfunction

Cardiac glycosides such as digoxin are Na+/K+-ATPase inhibitors that are widely used for the treatment of chronic heart failure and cardiac arrhythmias; however, recent epidemiological studies have suggested a relationship between digoxin treatment and increased mortality. We previously showed that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) ...

متن کامل

Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in apoE-deficient mice

Hyperhomocysteinemia (HHcy) has been shown to promote vascular inflammation and atherosclerosis, but the underlying mechanisms remain largely unknown. The NLRP3 inflammasome has been identified as the cellular machinery responsible for activation of inflammatory processes. In this study, we hypothesized that the activation of NLRP3 inflammasomes contributes to HHcy-induced inflammation and athe...

متن کامل

Nucleotide-binding oligomerization domain-like receptors and inflammasomes in the pathogenesis of non-microbial inflammation and diseases.

The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) or nucleotide-binding domain leucine-rich repeat-containing family of genes plays an important role in the development of innate immune responses. Some family members are known to form multiprotein complexes known as inflammasomes that regulate the processing and secretion of proinflammatory mediators, such as interleukin-1...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • American journal of cardiovascular disease

دوره 1 3  شماره 

صفحات  -

تاریخ انتشار 2011