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Medicinal plants have been used for the maintenance of human health since ancient times, in the form of food, spices, and traditional medicines. Medicinal plant-based traditional medicines serve as the primary healthcare systems in various countries even in recent times. Alongside this, medicinal plants have also served as the one of the main sources for the discovery of new therapeutic agents. At present, various plant extracts and their isolated phytochemicals are screened and evaluated for their diverse pharmacological activities related to both communicable and non-communicable diseases. However, comparatively little focus is given to the detailed mechanism of action of these agents on the molecular level. Molecular mechanism-based studies are essential for the development of evidence-based traditional medicines as well as for the development of isolated natural products as the lead candidates for novel drug discovery. This main focus of this Special Issue “Plant-based Bioactive Natural Products: Insights into Molecular Mechanisms of Action” is to cover the recent advances in science related to the molecular mechanisms of action of natural products. A total of nine articles were published in this Special Issue, including two original research articles and two review articles. This Special Issue has provided some new experimental data on bioactive natural products and their detailed mechanisms of action for biological activities. Similarly, review articles have provided state-of-the-art information on the related topics. I would like to thank all the authors for submitting their manuscripts and the reviewers and editors for their contribution to this Special Issue. Furthermore, I am also grateful to the handling editors and staffs of Applied Sciences for their support during the preparation and finalization of this Special Issue.

foodborne diseases --- giardiasis --- herbal drugs --- ethnobotany --- toxoplasmosis --- srophularia buergeriana --- cognitive impairment --- amyloid beta --- tau phosphorylation --- oxidative stress --- anti-apoptotic --- Terminalia chebula fruit --- osteoarthritis --- AyuFlex® --- cartilage collapse --- MMPs --- inflammation response --- vascular inflammation --- liensinine --- VSMC --- macrophage --- proliferation --- migration --- Nigella sativa --- methicillin-resistant --- Staphylococcus aureus --- synergism --- beta-lactam --- antibiotics --- artichoke by-products --- phenolic compounds --- HPLC-ESI-TOF-MS --- PLE --- GRAS --- Scrophularia buergeriana --- anti-amnesic effect --- cholinergic neurotransmission --- anti-oxidant --- anti-inflammation --- Vepris macropylla --- essential oil --- citral --- antiproliferative activity --- fluorescence and scanning electron microscopy --- human breast cancer cell line --- Vaccinium species --- phytochemicals --- berry --- leaf --- anti-inflammatory pathways --- endothelial dysfunction --- natural products --- bioactive compounds --- medicinal plants --- bioactivity --- mechanism of action --- traditional medicines

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Vascular smooth muscle (VSM) constitutes most of the tunica media in blood vessels and plays an important role in the control of vascular tone. Ca2+ is a major regulator of VSM contraction and is strictly regulated by an intricate system of Ca2+ mobilization and Ca2+ homeostatic mechanisms. The interaction of a physiological agonist with its plasma membrane receptor stimulates the hydrolysis of membrane phospholipids and increases the generation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 stimulates Ca2+ release from the intracellular stores in the sarcoplasmic reticulum. Agonists also stimulate Ca2+ influx from the extracellular space via voltage-gated, receptor-operated, and store-operated channels. Ca2+ homeostatic mechanisms tend to decrease the intracellular free Ca2+ concentration ([Ca2+]i) by activating Ca2+ extrusion via the plasmalemmal Ca2+ pump and the Na+/Ca2+ exchanger and the uptake of excess Ca2+ by the sarcoplasmic reticulum and possibly the mitochondria. A threshold increase in [Ca2+]i activates Ca2+-dependent myosin light chain (MLC) phosphorylation, stimulates actin-myosin interaction, and initiates VSM contraction. The agonist-induced maintained increase in DAG also activates specific protein kinase C (PKC) isoforms, which in turn cause phosphorylation of cytoplasmic substrates that increase the contractile myofilaments force sensitivity to Ca2+ and thereby enhance VSM contraction. Agonists could also activate Rho kinase (ROCK), leading to inhibition of MLC phosphatase and further enhancement of the myofilaments force sensitivity to Ca2+. The combined increases in [Ca2+]i, PKC and ROCK activity cause significant vasoconstriction and could also stimulate VSM hypertrophy and hyperplasia. The protracted and progressive activation of these processes could lead to pathological vascular remodeling and vascular disease.

Muscle contraction. --- Vascular diseases. --- Vascular smooth muscle. --- Ion Channels --- Muscle Proteins --- Microfilament Proteins --- Hemodynamics --- Muscle, Smooth --- Molecular Motor Proteins --- Cardiovascular Diseases --- Blood Vessels --- Diseases --- Muscles --- Contractile Proteins --- Cardiovascular Physiological Processes --- Cardiovascular System --- Adenosine Triphosphatases --- Membrane Glycoproteins --- Biopolymers --- Membrane Transport Proteins --- Cytoskeletal Proteins --- Polymers --- Tissues --- Carrier Proteins --- Acid Anhydride Hydrolases --- Proteins --- Cardiovascular Physiological Phenomena --- Membrane Proteins --- Anatomy --- Musculoskeletal System --- Amino Acids, Peptides, and Proteins --- Circulatory and Respiratory Physiological Phenomena --- Macromolecular Substances --- Hydrolases --- Chemicals and Drugs --- Phenomena and Processes --- Enzymes --- Enzymes and Coenzymes --- Myosins --- Muscle, Smooth, Vascular --- Vasoconstriction --- Calcium Channels --- Vascular Diseases --- Human Anatomy & Physiology --- Health & Biological Sciences --- Physiology --- Vascular resistance. --- Blood pressure. --- Vascular smooth muscle --- Physiology. --- physiology. --- Signal transduction --- Calcium --- Blood pressure --- AngII, angiotensin II --- ATP, adenosine triphosphate --- CPI-17, PKC-potentiated phosphatase inhibitor protein-17 kDa --- CAM, calmodulin --- DAG, diacylglycerol --- ET-1, endothelin --- IP3, inositol 1,4,5-trisphosphate --- MAPK, mitogen-activated protein kinase --- MARCKs, myristoylated alanine-rich C-kinase substrate --- MEK, MAPK kinase --- MLC, myosin light chain --- NCX, Na+-Ca2+ exchanger --- PDBu, phorbol 12,13-dibutyrate; PIP2, phosphatidylinositol 4,5-bisphosphate --- PKC, protein kinase C --- PMA, phorbol myristate acetate --- RACKs, receptors for activated C-kinase --- ROCK, Rho-kinase --- VSMC, vascular smooth muscle cell