After acute ischemic stroke (AIS), peripheral monocytes infiltrate into the lesion site within 24 h, peak at 3 to 7 days, and then differentiate into macrophages. Traditionally, monocytes/macrophages (MMs) are thought to play a deleterious role in AIS. Depletion of MMs in the acute phase can alleviate brain injury induced by ischemia. However, several studies have shown that MMs have anti-inflammatory functions, participate in angiogenesis, phagocytose necrotic neurons, and promote neurovascular repair. Therefore, MMs play dual roles in ischemic stroke, depending mainly upon the MM microenvironment and the window of time post-stroke. Because activated microglia and MMs are similar in morphology and function, previous studies have often investigated them together. However, recent studies have used special methods to distinguish MMs from microglia and have found that MMs have properties which differ from microglia. Here, we review the unique role of MMs and the interaction between MMs and neurovascular units, including neurons, astrocytes, microglia, and microvessels. Future therapeutics targeting MMs should regulate the polarization and subset transformation of the MMs at different stages of AIS rather than comprehensively suppressing MM infiltration and differentiation. In addition, more studies are needed to elucidate the cellular and molecular mechanisms of MM subsets and polarization during ischemic stroke.

急性缺血性中风（AIS）后，外周单核细胞在24小时内浸润到病变部位，在3至7天达到峰值，然后分化为巨噬细胞。传统上，单核细胞/巨噬细胞（MM）被认为在AIS中起有害作用。急性期MMs的耗竭可以减轻缺血引起的脑损伤。但是，一些研究表明，MM具有抗炎功能，参与血管生成，吞噬坏死性神经元并促进神经血管修复。因此，MM在缺血性中风中起双重作用，主要取决于MM的微环境和中风后的时间窗口。由于活化的小胶质细胞和MM在形态和功能上相似，因此以前的研究经常将它们一起研究。然而，最近的研究已使用特殊方法将MM与小胶质细胞区分开，并发现MM具有与小胶质细胞不同的特性。在这里，我们回顾了MM的独特作用以及MM与神经血管单位（包括神经元，星形胶质细胞，小胶质细胞和微血管）之间的相互作用。未来针对MM的疗法应在AIS的不同阶段调节MM的极化和亚群转化，而不是全面抑制MM的浸润和分化。此外，还需要更多的研究来阐明缺血性卒中期间MM亚群和极化的细胞和分子机制。和微血管。未来针对MM的疗法应在AIS的不同阶段调节MM的极化和亚群转化，而不是全面抑制MM的浸润和分化。此外，还需要更多的研究来阐明缺血性卒中期间MM亚群和极化的细胞和分子机制。和微血管。未来针对MM的疗法应在AIS的不同阶段调节MM的极化和亚群转化，而不是全面抑制MM的浸润和分化。此外，还需要更多的研究来阐明缺血性卒中期间MM亚群和极化的细胞和分子机制。