Cardiovascular Drugs and Osteoarthritis: Effects of Targeting Ion Channels
Abstract
:1. Introduction
2. The Association between OA and CVD
2.1. Risk Factors for OA and CVD
2.1.1. Common Risk Factors for OA and CVD
2.1.2. Distinct Risk Factors for CVD and OA
2.2. Oxidative Stress and Other Common Molecular Mechanisms in CVD and OA
3. Ion Channel Regulators for the Treatment of CVD
4. Cardiovascular Drugs Directly and Indirectly Regulating Ion Channels
4.1. Inhibitors of Voltage-Gated Calcium (Ca2+) Channels in Chondrogenesis
4.2. Voltage-Gated Sodium (Na+) Channels in Chondrogenesis
4.3. Potassium (K+) Channels in CVD and Chondrocytes Metabolism
4.4. Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Channels
4.5. Complex Activity of Ion Channel Regulators
5. CVD Drugs Indirectly Regulating Ion Channels
5.1. Non-Selective Inhibitors of β-Adrenergic System
5.2. Modulators of Renin-Angiotensin-Aldosterone System (RAAS)
6. Conclusions
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
References
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Drug | Role in CVD | Effect on Cartilage In Vitro | Effect on Cartilage in Animal Models In Vivo | Effect on Patients | References |
---|---|---|---|---|---|
Direct ion channel modulators | |||||
Voltage-Gated Calcium Channel Blockers | |||||
Verapamil | Inhibits VGCC in vascular smooth muscle and myocardial tissue, reduces peripheral vascular resistance and heart contractility. Indications: hypertension, chest angina, arrhythmia | Inhibition of chondrocyte proliferation, decreased number of hypertrophic chondrocytes, upregulation of chondrogenic markers (ACAN, COL2A1, SOX9), downregulation of AXIN2 and MMP3 in human osteoarthritic chondrocytes | - | Worsened OA patients’ condition based on Lequesne scoring system | [123,124,125] |
Nifedipine | Inhibits VGCC in vascular smooth muscle cells, causing smooth muscle relaxation and decrease of blood pressure. Indications: hypertension, chest angina | Inhibition of chondrocyte maturation and proliferation in bone marrow-mesenchymal stem cells and chondrocytes; upregulated production of GAGs and collagen type II in human chondrocytes | - | No effects in OA patients according to Lequesne scoring system | [124,126] |
Amlodipine, lercanidipine, felodipine, nitrendipine | - | - | Improved Lequesne index in OA patients | [124] | |
Voltage-Gated Sodium Channel Blockers | |||||
Lidocaine | Inhibits VGSC, decreases the depolarization, automaticity and excitability in the ventricles Indication: arrhythmia | Chondrotoxic effect; necrosis in equine and bovine articular chondrocytes | - | Reduced pain in OA patients | [127,128,129] |
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Inhibitors | |||||
Ivabradine | Lowers heart rate by selectively inhibiting If channels (“funny channels”) in the heart and prolonging diastolic depolarization Indication: heart failure | Reduced expression of matrix metalloproteinases (MMP-3 and MMP-13), ADAMTS-4 and ADAMTS-5 in primary human chondrocytes | - | - | [130] |
Indirect ion channel modulators | |||||
β-adrenoreceptor Inhibitors | |||||
Propranolol | Nonselective β-adrenergic receptor antagonist Indications: hypertension, angina, arrhythmia | Promoted chondrogenic differentiation to hypertrophic chondrocytes by increasing Col I and Col X gene expression, decreasing SOX6 expression in murine pre-chondrogenic ATDC5 cells; suppressed subchondral bone loss in rat model. | - | - | [131,132] |
Carvedilol | Reversed IL-1β induced downregulation of aggrecan and Col II protein in murine pre-chondrogenic ATDC5 cells in SW1353 chondrocytes | - | - | [133,134] | |
Angiotensin-Aldosterone System Modulators | |||||
Captopril | Inhibitor of angiotensin-converting enzyme Indications: hypertension, heart failure | Inhibited reversion of procollagen to collagen in cartilage and tendon cell culture | Increased thickness of articular cartilage, decreased hypertrophic zone and increased proliferative zone in rat OA model | - | [135,136,137,138] |
Enalapril | Inhibited reversion of procollagen to collagen in cartilage and tendon cell culture | - | - | [135] | |
Losartan | Angiotensin II receptor inhibitor Indications: hypertension, heart failure | - | Increased OA progression according to histopathological scoring in murine OA model; increased Col10a1 expression in mice; diminished degradation of cartilage in mice; enhanced hyaline-like rabbit cartilage healing | - | [139,140,141,142] |
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Vaiciuleviciute, R.; Bironaite, D.; Uzieliene, I.; Mobasheri, A.; Bernotiene, E. Cardiovascular Drugs and Osteoarthritis: Effects of Targeting Ion Channels. Cells 2021, 10, 2572. https://doi.org/10.3390/cells10102572
Vaiciuleviciute R, Bironaite D, Uzieliene I, Mobasheri A, Bernotiene E. Cardiovascular Drugs and Osteoarthritis: Effects of Targeting Ion Channels. Cells. 2021; 10(10):2572. https://doi.org/10.3390/cells10102572
Chicago/Turabian StyleVaiciuleviciute, Raminta, Daiva Bironaite, Ilona Uzieliene, Ali Mobasheri, and Eiva Bernotiene. 2021. "Cardiovascular Drugs and Osteoarthritis: Effects of Targeting Ion Channels" Cells 10, no. 10: 2572. https://doi.org/10.3390/cells10102572
APA StyleVaiciuleviciute, R., Bironaite, D., Uzieliene, I., Mobasheri, A., & Bernotiene, E. (2021). Cardiovascular Drugs and Osteoarthritis: Effects of Targeting Ion Channels. Cells, 10(10), 2572. https://doi.org/10.3390/cells10102572