The thioredoxin system, which consists of thioredoxin (Trx), nicotinamide adenine dinucleotide phosphate (NADPH) and thioredoxin reductase (TrxR), has emerged as a major anti-oxidant involved in the maintenance of cellular physiology and survival. Dysregulation in this system has been associated with metabolic, cardiovascular, and malignant disorders. Thioredoxin-interacting protein (TXNIP), also known as vitamin D-upregulated protein or thioredoxin-binding-protein-2, functions as a physiological inhibitor of Trx, and pathological suppression of Trx by TXNIP has been demonstrated in diabetes and cardiovascular diseases. Furthermore, TXNIP effects are partially Trx-independent; these include direct activation of inflammation and inhibition of glucose uptake. Many of the effects of TXNIP are initiated by its dissociation from intra-nuclear binding with Trx or other SH-containing proteins: these effects include its migration to cytoplasm, modulating stress responses in mitochondria and endoplasmic reticulum, and also potentially activating apoptotic pathways. TXNIP also interacts with the nitric oxide (NO) signaling system, with apparent suppression of NO effect. TXNIP production is modulated by redox stress, glucose levels, hypoxia and several inflammatory activators. In recent studies, it has been shown that therapeutic agents including insulin, metformin, angiotensin converting enzyme inhibitors and calcium channel blockers reduce TXNIP expression, although it is uncertain to what extent TXNIP suppression contributes to their clinical efficacy. This review addresses the role of TXNIP in health and in cardiovascular and metabolic disorders. Finally, the potential advantages (and disadvantages) of pharmacological suppression of TXNIP in cardiovascular disease and diabetes are summarized.

TTC is associated acutely with a marked increase in GCS. Potentially, GCS might contribute to increased coronary vascular permeability in TTC, thus dissociating development of myocardial oedema from severity of associated inflammation. Prevention of GCS represents a potential therapeutic option in TTC.

The compounds involved in the hydroxycinnamic acid amide (HCAA) pathway are an important class of metabolites in plants. Extensive studies have reported that a variety of plant hydroxycinnamamides exhibit pivotal roles in plant–pathogen interactions, such as p-coumaroylagmatine and ferulic acid. The aim of this review is to discuss the emerging findings on the functions of hydroxycinnamic acid amides (HCAAs) accumulation associated with plant defenses against plant pathologies, antimicrobial activity of HCAAs, and the mechanism of HCAAs involved in plant immune responses (such as reactive oxygen species (ROS), cell wall response, plant defense hormones, and stomatal immunity). However, these advances have also revealed the complexity of HCAAs participation in plant defense reactions, and many mysteries remain to be revealed. This review provides an overview of the mechanistic and conceptual insights obtained so far and highlights areas for future exploration of phytochemical defense metabolites.