When Monocytes Come (Too) Close to Our Hearts

Cardilo-Reis, Larissa; Witztum, Joseph L.; Binder, Christoph J.

doi:10.1016/j.jacc.2009.11.068

Cited by 7 publications

(2 citation statements)

References 12 publications

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“…(Alkhouli et al., 2020; Tsao et al., 2023) Early revascularization after an MI by coronary bypass graft (CABG) surgery or percutaneous coronary intervention (PCI; angioplasty with stent) is the most effective strategy to salvage myocardium, reduce infarct size, and prevent HF. (Hausenloy & Yellon, 2013; Neri et al., 2017; O'Neill et al., 1986) However, restoration of blood flow to the oxygen‐deprived heart generates energetic imbalances, oxidative stress, and a massive inflammatory response that further damages the heart, (Cardilo‐Reis et al., 2010) a paradox termed “myocardial ischemia and reperfusion injury” (IRI). (Nahrendorf et al., 2007; Panizzi et al., 2010) These biological cues dictate the size of the initial infarct and quality of infarct healing, key elements that determine long‐term survival and progression to HF.…”

Section: Introductionmentioning

confidence: 99%

Epicardial placement of human placental membrane protects from heart injury in a swine model of myocardial infarction

Skaria,

Lopez‐Pier,

Kathuria

et al. 2023

Physiological Reports

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Cardiac ischemic reperfusion injury (IRI) is paradoxically instigated by reestablishing blood‐flow to ischemic myocardium typically from a myocardial infarction (MI). Although revascularization following MI remains the standard of care, effective strategies remain limited to prevent or attenuate IRI. We hypothesized that epicardial placement of human placental amnion/chorion (HPAC) grafts will protect against IRI. Using a clinically relevant model of IRI, swine were subjected to 45 min percutaneous ischemia followed with (MI + HPAC, n = 3) or without (MI only, n = 3) HPAC. Cardiac function was assessed by echocardiography, and regional punch biopsies were collected 14 days post‐operatively. A deep phenotyping approach was implemented by using histological interrogation and incorporating global proteomics and transcriptomics in nonischemic, ischemic, and border zone biopsies. Our results established HPAC limited the extent of cardiac injury by 50% (11.0 ± 2.0% vs. 22.0 ± 3.0%, p = 0.039) and preserved ejection fraction in HPAC‐treated swine (46.8 ± 2.7% vs. 35.8 ± 4.5%, p = 0.014). We present comprehensive transcriptome and proteome profiles of infarct (IZ), border (BZ), and remote (RZ) zone punch biopsies from swine myocardium during the proliferative cardiac repair phase 14 days post‐MI. Both HPAC‐treated and untreated tissues showed regional dynamic responses, whereas only HPAC‐treated IZ revealed active immune and extracellular matrix remodeling. Decreased endoplasmic reticulum (ER)‐dependent protein secretion and increased antiapoptotic and anti‐inflammatory responses were measured in HPAC‐treated biopsies. We provide quantitative evidence HPAC reduced cardiac injury from MI in a preclinical swine model, establishing a potential new therapeutic strategy for IRI. Minimizing the impact of MI remains a central clinical challenge. We present a new strategy to attenuate post‐MI cardiac injury using HPAC in a swine model of IRI. Placement of HPAC membrane on the heart following MI minimizes ischemic damage, preserves cardiac function, and promotes anti‐inflammatory signaling pathways.

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Section: Introductionmentioning

confidence: 99%

Epicardial placement of human placental membrane protects from heart injury in a swine model of myocardial infarction

Skaria,

Lopez‐Pier,

Kathuria

et al. 2023

Physiological Reports

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show abstract

“…14,15 They facilitate the healing process by removing dead cells, as well as by secreting trophic, angiogenic, and profibrotic cytokines, chemokines, and proteases. 15,17 These healing properties are attributed to distinct monocyte and macrophage subsets. 14,16,[18][19][20] Thus, control of macrophage function could be a major therapeutic target in directing the process of infarct repair.…”

Section: Introductionmentioning

confidence: 99%

Targeting Macrophage Subsets for Infarct Repair

Ben-Mordechai

Palevski

Glucksam-Galnoy

et al. 2014

J Cardiovasc Pharmacol Ther

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Macrophages are involved in every cardiovascular disease and are an attractive therapeutic target. Macrophage activation is complex and can be either beneficial or deleterious, depending upon its mode of action, its timing, and its duration. An important macrophage characteristic is its plasticity, which enables it to switch from one subset to another. Macrophages, which regulate healing and repair after myocardial infarction, have become a major target for both treatment and diagnosis (theranostic). The aim of the present review is to describe the recent discoveries related to targeting and modulating of macrophage function to improve infarct repair. We will briefly review macrophage polarization, plasticity, heterogeneity, their role in infarct repair, regeneration, and cross talk with mesenchymal cells. Particularly, we will focus on the potential of macrophage targeting in situ by liposomes. The ability to modulate macrophage function could delineate pathways to reactivate the endogenous programs of myocardial regeneration. This will eventually lead to development of small molecules or biologics to enhance the endogenous programs of regeneration and repair.

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Cardiac MRI Assessment of Mouse Myocardial Infarction and Regeneration

2020

Methods in Molecular Biology

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When Monocytes Come (Too) Close to Our Hearts

Cited by 7 publications

References 12 publications

Epicardial placement of human placental membrane protects from heart injury in a swine model of myocardial infarction

Epicardial placement of human placental membrane protects from heart injury in a swine model of myocardial infarction

Targeting Macrophage Subsets for Infarct Repair

Cardiac MRI Assessment of Mouse Myocardial Infarction and Regeneration

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