Abstract
Inflammasomes are multiprotein complexes with an important role in the innate immune response. Canonical activation of inflammasomes results in caspase-1 activation and maturation of cytokines interleukin-1β and -18. These cytokines can elicit their effects through receptor activation, both locally within a certain tissue and systemically. Animal models of kidney diseases have shown inflammasome involvement in inflammation, pyroptosis and fibrosis. In particular, the inflammasome component nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) and related canonical mechanisms have been investigated. However, it has become increasingly clear that other inflammasome components are also of importance in kidney disease. Moreover, it is becoming obvious that the range of molecular interaction partners of inflammasome components in kidney diseases is wide. This review provides insights into these current areas of research, with special emphasis on the interaction of inflammasome components and redox signalling, endoplasmic reticulum stress, and mitochondrial function. We present our findings separately for acute kidney injury and chronic kidney disease. As we strictly divided the results into preclinical and clinical data, this review enables comparison of results from those complementary research specialities. However, it also reveals that knowledge gaps exist, especially in clinical acute kidney injury inflammasome research. Furthermore, patient comorbidities and treatments seem important drivers of inflammasome component alterations in human kidney disease.
Highlights
Introduction to Kidney Disease andInflammation in Kidney DiseaseThe 2020 analysis of the Global Burden of Disease Study 1990–2017 estimated the global prevalence of chronic kidney disease (CKD) to be 9.1%, corresponding to697.5 million cases [1,2]
We demonstrated the considerable diversity of the inflammasome components and their interactions with various molecular partners involved in kidney disease pathophysiology
Reactive oxygen species contribute to inflammasome priming and activation, while mitochondria and ER stress both contribute to the activation of NLRP3 inflammasomes
Summary
The 2020 analysis of the Global Burden of Disease Study 1990–2017 estimated the global prevalence of chronic kidney disease (CKD) to be 9.1%, corresponding to. Inflammatory and immunological processes are intimately linked to kidney disease They contribute to the initiation of injury in AKI, for example during sepsis, and play an important role for AKI’s extension and maintenance phase [4], and AKI-to-CKD transition [5]. Inflammatory and immunological processes are involved in a wide range of CKD causes, like diabetes mellitus or systemic lupus erythematosus. They contribute to CKD progression, independent of the underlying cause [6]. Excellent reviews have been published on the topic, reporting inflammasome taxonomy and tissue expression pattern, molecular mechanisms of inflammasome activation and function, respective renal disease models, roles in human kidney disease, inflammasome gene mutations and polymorphisms, and inflammasome-related therapeutic options, such as the Refs.
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