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In addition, along the same line, endogenous specialized pro-resolving mediators have been identified as regulators of infection and inflammation [ 77 ]. For example, activation of NRs by a variety of endo- and exogenous chemicals are elemental to induction and repression of drug-metabolism pathways.

The master xenobiotic-sensing NRs, the promiscuous pregnane X receptor PXR , and less-promiscuous constitutive androstane receptor CAR are crucial to initial ligand recognition, jump-starting the metabolic process [ 78 ]. In addition, phytoestrogens are natural endocrine disruptors that interfere with estrogenic pathways. Moreover, bisphenol A BPA is widely used as a component in polycarbonate plastics for food and beverage packaging, epoxy linings for canned foods, and dental sealants, among other applications. The most widely accepted speculation is that both narrow and broad specificity seen for receptors or proteins are a result of natural selection process [ 81 ].

Less specificity of receptors provides evolutionary advantage to organisms that had to conduct a broad set of biological activities with limited protein repertoire and also allowed the organisms to evolve new responses to many endogenous and external ligands [ 82 , 83 , 84 ].

Promiscuity of such receptors complicate identification of the physiological ligands that activate them in vivo [ 85 ]. One way to identify candidate ligands for orphan NRs is to identify their three dimensional structure [ 86 , 87 ]. However, receptor affinity for the ligand and the physiological concentrations of the ligand in the tissues have to be taken into account when determining the potential relevance of the specific ligand for the receptor function [ 85 , 88 ].

Additionally, if it is known that the promiscuous NRs require intracellular lipid binding proteins to shuttle the ligand toward it like PPAR utilizing certain FABPs—fatty acid binding proteins , the nuclear translocation of the particular protein in response to a compound can be used to determine potential ligands for the NR [ 85 ]. Nevertheless, identifying the potential endogenous ligands bound to the NR of interest in vivo by using mass spectroscopy, high-performance liquid chromatography HPLC or gas chromatography are the most relevant methods than the ones mentioned above [ 85 , 89 , 90 ].

We acknowledge that some of the fold changes shown in our tables are less than twofold. However, complex diseases such as diabetes, obesity, cancer, and autoimmune disorders are regulated by myriad of genes similar to quantitative traits [ 91 , 92 ]. Previously, for most of the continuous traits, the strongest genetic association could explain only a small fraction of the genetic variance [ 93 , 94 ].

However, later analyses revealed that casual loci with small effect size are also important in determining continuous traits and complex diseases such as schizophrenia [ 94 ]. Moreover, recent publications demonstrated that complex and chronic diseases are driven by accumulation of weak effects on the key genes and regulatory pathways [ 95 , 96 ].

It is evident that polygenic effects are important across a wide variety of traits and diseases such as diabetes [ 97 ]. Therefore, it is our understanding that even a low fold change in potent transcription factors such as NRs can significantly impact progression of complex diseases.

T cell co-stimulation and co-inhibition in cardiovascular disease: a double-edged sword

To improve our understanding on most NRs as anti-inflammatory sensors and regulators, we propose a new working model and classified most NRs as homeostasis-associated molecular pattern receptors HAMPRs as shown in Fig. Vascular inflammation and atherogenesis are activated via receptors for PAMPs and suppressed by regulatory t cells.

Drug Discov Today Ther Strateg. Inflammasomes are differentially expressed in cardiovascular and other tissues.

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