Table 3 Selected published articles related to the current status of preclinical macrophage targeting strategies
From: Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets
Study | Model | Therapeutic strategy | Therapeutic outcome | Citation |
|---|---|---|---|---|
Inhibition of macrophage recruitment | ||||
Ostermann et al. (2005) | AS | JAM-A inhibition | Soluble JAM-A inhibits JAM-A mediated recruitment of monocytes on atherosclerotic endothelium and reduces inflammation, thereby reducing the formation of atherosclerosis. | |
Kentischer et al. (2006) | AS | Anti-MIF monoclonal antibody treatment | MIF blockade strongly reduces macrophage content in the lesions and leads to markedly decreased levels of circulating and local aortic inflammatory mediators, thereby reducing the formation of atherosclerosis. | |
Christophe et al. (2008) | AS | Combined inhibition of CCL2, CX3CR1, and CCR5 | Combined inhibition of CCL2, CX3CR1, and CCR5 pathways almost abrogates macrophage accumulation and atherosclerosis in mice. | |
Wang et al. (2018) | MI | Anti-CCR2 antibody treatment | Inhibiting CCR2 significantly reduces monocyte recruitment in the heart, alleviates inflammatory cascade reactions, and reduces myocardial infarction area. | |
Samuel et al. (2023) | AS | VCAM-1 Inhibition | RAG8 treatment reduces VCAM-1 protein levels and platelet accumulation in atherosclerotic coronary arteries, thereby reducing coronary artery atherosclerosis and myocardial fibrosis. | |
Inhibition of foam cell formation and macrophage survival | ||||
Andrew et al. (2004) | AS | Inducing ABCA1 expression | PPARα and PPARγ agonist therapy induces LXRα and LXR mediated ABCA1 expression which plays a role in promoting cholesterol efflux and reducing the formation of foam cells, ultimately inhibiting the development of atherosclerosis. | |
Secchiero et al. (2006) | AS | TRAIL injection | TRAIL injection not only significantly attenuates the total extension of the plaques, but also contributes to stabilize atherosclerotic plaques by selectively decreasing the number of infiltrating macrophages in the atherosclerotic lesions. | |
Verheye et al. (2007) | AS | Delivery of everolimus | Stent-based delivery of everolimus selectively clears macrophages in rabbit atherosclerotic plaques by autophagy, thereby reduceing atherosclerosis. | |
Petri et al. (2010) | AS | Silence of SR-A | Silencing of SR-A significantly reduces the formation of foam cells, thereby reducing atherosclerosis in mice. | |
Duewell et al. (2010) | AS | NLRP3-deficient | The absence of NLRP3 inflammasome significantly protects atherosclerotic mice from disease invasion and reduces the size of lesions. | |
Wang et al. (2013) | AS | Downregulation of mTOR expression | The down-regulation of mTOR induces autophagy of macrophages, leading to a decrease in their number and stabilizing atherosclerotic plaque. | |
Zhai et al. (2014) | AS | Inhibition of PI3K/Akt/mTOR signaling pathway | Selective inhibition of Akt/mTOR signaling pathway reduces macrophages by promoting autophagy, thereby stabilizing vulnerable atherosclerotic plaque. | |
Karunakaran et al. (2016) | AS | Nec-1 treatment | Nec-1 reduces lesion size and markers of plaque instability, including necrotic core formation. | |
Shoulders et al. (2019) | AS | Clo-Lip administration | Clo-Lip administration leads to macrophage apoptosis by inhibiting mitochondrial oxygen consumption, thus preventing the progression of atherosclerosis. | |
Xu et al. (2023) | AS | IL-37 treatment | IL-37 inhibits iron death of macrophages by activating the NRF2 pathway, thereby slowing down the progression of atherosclerosis. | |
Luo et al. (2024) | AS | MCL treatment | MCL activates the NRF2 pathway, thereby inhibiting ferroptosis of macrophages and alleviating the progression of atherosclerosis. | |
Regulation of macrophage function | ||||
Cardilo-Reis et al. (2012) | AS | IL-13 treatment | IL-13 promotes the production of repair macrophages, thereby stabilizing AS plaques and preventing the development of AS. | |
Sager et al. (2015) | MI | Anti-IL-1β treatment | Anti-IL-1β reduces leukocyte infiltration, reduces inflammation in the infarct area, weakens fibrosis, and prevents adverse cardiac remodeling. | |
Wei et al. (2015) | AS | MiR-155 inhibition | MiR-155 inhibition promotes macrophage efferocytosis, thereby inhibiting the formation of necrotic core and the progression of atherosclerosis. | |
Brenner et al. (2015) | AS | Sitagliptin treatment | Sitagliptin promotes the differentiation of monocytes into the M2 phenotype, reduces plaque burden, and thereby inhibiting early atherosclerosis. | |
Gabunia et al. (2016) | AS | IL-19 treatment | IL-19 inhibits macrophage inflammation, maintains cholesterol homeostasis, thereby preventing AS plaque progression. | |
Jung et al. (2017) | MI | IL-10 treatment | Infusion of IL-10 at the appropriate period can inhibit post-MI inflammation and reduce collagen deposition by stimulating the polarization of M2 macrophages. | |
Price et al. (2017) | AS | MiR-33 inhibition | Anti-miR-33 therapy reduces lipid accumulation and inflammatory responses in macrophages, thereby mediating AS protection. | |
Lee et al. (2017) | MI | Dapagliflozin treatment | Dapagliflozin increases the activation of M2 macrophages, thereby inhibiting the differentiation of myofibroblasts and reducing collagen fiber production and alleviating myocardial fibrosis. | |
Han et al. (2018) | MI | IL-4pDNA treatment | IL-4pDNA delivery promotes M2 polarization, which reduces cardiac inflammation, weakens fibrosis, and improves cardiac function. | |
Jin et al. (2018) | AS | MiR-21 treatment | MiR-21 inhibits the transformation of macrophages into foam cells and relieves the restriction of smooth muscle cells proliferation by activated macrophages, which results in thickening of the fibrous cap and stabilization of AS plaques. | |
Podaru et al. (2019) | MI | M-CSF and IL-4-induced macrophage transplantation | Cardiac microvascular formation is enhanced, cardiomyocyte hypertrophy is reduced, and pathological interstitial fibrosis distal to the infarcted area is attenuated. | |
Tokutome et al. (2019) | MI | Pioglitazone treatment | Pioglitazone increases M2 macrophage activation, reduces cardiac inflammatory response, and promotes appropriate collagen fiber production. | |
Liao et al. (2020) | MI | Heart-derived MSCs infusion | MSCs infusion inhibits macrophage infiltration and induces the development of macrophages toward an anti-inflammatory M2 phenotype, significantly reducing infarct size after AMI and mediating appropriate fibrogenesis in the injured area. | |
Zhang et al. (2021) | AS | Rosuvastatin treatment | Rosuvastatin improves macrophage autophagy activity and lipid accumulation, thereby exerting anti-atherosclerotic effects. | |
Zhu et al. (2022) | MI | Hypoxia-induced macrophage transplantation | Myocardial cell apoptosis is reduced, angiogenesis is induced, and fibrosis in the infarct area and border zone is attenuated. | |
Abdollahi et al. (2022) | AS | Dapagliflozin treatment | Dapagliflozin can inhibit the inflammatory response of macrophages, thereby preventing the progression of AS. | |
Chen et al. (2023) | MI | IL-4pDNA treatment | IL-4pDNA promotes M2 polarization, reduces cardiac inflammation, promotes cardiac angiogenesis, and alleviates myocardial fibrosis. | |
Wang et al. (2023) | MI | IL-10 treatment | IL-10 delivery promotes M2 polarization, reduces cardiac inflammation, and effectively reduces myocardial fibrosis in the infarct area. | |
