Abstract
Osteoarthritis (OA) and cardiovascular diseases (CVD) share many similar features, including similar risk factors and molecular mechanisms. A great number of cardiovascular drugs act via different ion channels and change ion balance, thus modulating cell metabolism, osmotic responses, turnover of cartilage extracellular matrix and inflammation. These drugs are consumed by patients with CVD for many years; however, information about their effects on the joint tissues has not been fully clarified. Nevertheless, it is becoming increasingly likely that different cardiovascular drugs may have an impact on articular tissues in OA. Here, we discuss the potential effects of direct and indirect ion channel modulating drugs, including inhibitors of voltage gated calcium and sodium channels, hyperpolarization-activated cyclic nucleotide-gated channels, β-adrenoreceptor inhibitors and angiotensin-aldosterone system affecting drugs. The aim of this review was to summarize the information about activities of cardiovascular drugs on cartilage and subchondral bone and to discuss their possible consequences on the progression of OA, focusing on the modulation of ion channels in chondrocytes and other joint cells, pain control and regulation of inflammation. The implication of cardiovascular drug consumption in aetiopathogenesis of OA should be considered when prescribing ion channel modulators, particularly in long-term therapy protocols.
Highlights
OA is a whole joint disease, and since the synovial joint is regarded as an organ, many constituent tissues are affected, including articular cartilage [3], subchondral bone [4,5,6], synovium [7,8,9], infrapatellar fat pad [10,11], meniscus [12] and intraarticular ligaments [13]
Cardiovascular drugs are systemically administered for long periods of time and may affect myocardium or smooth vascular muscles and can interact with ion channels on the cells of other organs, including subchondral bone, synovium and articular cartilage
Several types of potassium channels were identified in chondrocytes, including adenosine triphosphate (ATP)-sensitive (KATP), voltage-gated potassium channels (VGPC), calcium-activated potassium channels (KCa), of 23 inward rectifier potassium channels (Kir), potassium channels and tandem pore10potassium channels (K2P) [157]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The aim of this review is to discuss the potential effects of currently used CVD drugs on cartilage, synovium and subchondral bone, focusing on their mechanisms of action on ion channels in joint cells, pain control, regulation of inflammation and possible consequences on the progression of OA. OA and CVD, showing that the anti-inflammatory medicine canakinumab hyperglycaemia and increased waist fat are components of the metabolic syndrome reduced cardiovascular event rates together with incidence rates of total hip total knee [45] It which is one of the main risk factors for OA with a metabolic diseaseorphenotype replacement [44].
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