Piezoelectric materials, with their unique ability for mechanical‐electrical energy conversion, have been widely applied in important fields such as sensing, energy harvesting, wastewater treatment, and catalysis. In recent years, advances in material synthesis and engineering have provided new opportunities for the development of bio‐piezoelectric materials with excellent biocompatibility and piezoelectric performance. Bio‐piezoelectric materials have attracted interdisciplinary research interest due to recent insights on the impact of piezoelectricity on biological systems and their versatile biomedical applications. This review therefore introduces the development of bio‐piezoelectric platforms from a broad perspective and highlights their design and engineering strategies. State‐of‐the‐art biomedical applications in both biosensing and disease treatment will be systematically outlined. The relationships between the properties, structure, and biomedical performance of the bio‐piezoelectric materials are examined to provide a deep understanding of the working mechanisms in a physiological environment. Finally, the development trends and challenges are discussed, with the aim to provide new insights for the design and construction of future bio‐piezoelectric materials.

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Abstract-We investigated the effects of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (statin) on the inhibitory effects of an angiotensin II type-1 receptor (AT 1 ) blocker on atherosclerosis and explored cellular mechanisms. We gave apolipoprotein E null mice a high-cholesterol diet for 10 weeks and measured atherosclerotic plaque area and lipid deposition. Neither 1 mg/kg per day of valsartan nor 3 mg/kg per day of fluvastatin had any effect on blood pressure or cholesterol concentration; however, both drugs decreased plaque area and lipid deposition after 10 weeks. We then reduced the doses of both drugs to 0.1 mg/kg per day and 1 mg/kg per day, respectively. At these doses, neither drug had an effect on atherosclerotic lesions. When both drugs were combined at these doses, a significant reduction in atherosclerotic lesions was observed. Similar inhibitory effects of valsartan or fluvastatin on the expressions of nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide phosphate oxidase subunits p22 phox and p47 phox , production of superoxide anion, the expression of monocyte chemoattractant protein-1, and intercellular adhesion molecule-1 expression were observed. These results suggest that concomitant AT 1 receptor and cholesterol biosynthesis blockade, particularly when given concomitantly, blunts oxidative stress and inflammation independent of blood pressure or cholesterol-related effects. Key Words: angiotensin Ⅲ atherosclerosis Ⅲ oxidative stress T he angiotensin II (Ang II) type-1 (AT 1 ) receptor mediates the major cardiovascular actions of Ang II. AT 1 receptor blockers (ARBs) putatively exert a vascular protective effect. 1 We reported previously that the ARB valsartan attenuated neointimal formation, decreased vascular smooth muscle cell (VSMC) proliferation, and diminished vascular inflammation. 2 On the other hand, recent large clinical trials showed that 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) decreased ischemic stroke, myocardial infarction, and mortality in hypercholesterolemic subjects. Possibly, some of the statin-related beneficial effects may be cholesterol independent. 3,4 Statins may prevent Ang IIinduced cellular and organ damage. [5][6][7][8] We demonstrated previously that neointimal formation and VSMC proliferation induced by cuff placement around the femoral artery were significantly inhibited by a valsartan-fluvastatin combination. Either drug alone at these doses did not affect neointimal formation or VSMC proliferation. 9 The drug combination showed a more effective reduction in medial cross-sectional area in genetically hypertensive rats than either drug alone. Furthermore, valsartan showed additive antioxidative effects when given with fluvastatin in terms of LDL oxidation in hypercholesterolemic and hypertensive patients compared with monotherapy. 10,11 We conceived an experimental study to explore the mechanisms involved with the combination therapy. We studied apolipoprotein E-deficient knockout (ApoEKO) mice, which de...

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