Injectable Hydrogels for Cardiac Tissue Regeneration Post-Myocardial Infarction

Author(s):  
G. N. Grover ◽  
K. L. Christman
2015 ◽  
Vol 2 (11) ◽  
pp. 1500122 ◽  
Author(s):  
Anwarul Hasan ◽  
Ahmad Khattab ◽  
Mohammad Ariful Islam ◽  
Khaled Abou Hweij ◽  
Joya Zeitouny ◽  
...  

2020 ◽  
Vol 21 (17) ◽  
pp. 5952 ◽  
Author(s):  
Saltanat Smagul ◽  
Yevgeniy Kim ◽  
Aiganym Smagulova ◽  
Kamila Raziyeva ◽  
Ayan Nurkesh ◽  
...  

Myocardial infarction causes cardiac tissue damage and the release of damage-associated molecular patterns leads to activation of the immune system, production of inflammatory mediators, and migration of various cells to the site of infarction. This complex response further aggravates tissue damage by generating oxidative stress, but it eventually heals the infarction site with the formation of fibrotic tissue and left ventricle remodeling. However, the limited self-renewal capability of cardiomyocytes cannot support sufficient cardiac tissue regeneration after extensive myocardial injury, thus, leading to an irreversible decline in heart function. Approaches to improve cardiac tissue regeneration include transplantation of stem cells and delivery of inflammation modulatory and wound healing factors. Nevertheless, the harsh environment at the site of infarction, which consists of, but is not limited to, oxidative stress, hypoxia, and deficiency of nutrients, is detrimental to stem cell survival and the bioactivity of the delivered factors. The use of biomaterials represents a unique and innovative approach for protecting the loaded factors from degradation, decreasing side effects by reducing the used dosage, and increasing the retention and survival rate of the loaded cells. Biomaterials with loaded stem cells and immunomodulating and tissue-regenerating factors can be used to ameliorate inflammation, improve angiogenesis, reduce fibrosis, and generate functional cardiac tissue. In this review, we discuss recent findings in the utilization of biomaterials to enhance cytokine/growth factor and stem cell therapy for cardiac tissue regeneration in small animals with myocardial infarction.


2020 ◽  
Vol 127 (11) ◽  
pp. 1422-1436
Author(s):  
Adele L. Richart ◽  
Medini Reddy ◽  
Mina Khalaji ◽  
Alaina L. Natoli ◽  
Sarah E. Heywood ◽  
...  

Rationale: Decades of research have examined immune-modulatory strategies to protect the heart after an acute myocardial infarction and prevent progression to heart failure but have failed to translate to clinical benefit. Objective: To determine anti-inflammatory actions of n-apo AI (Apo AI nanoparticles) that contribute to cardiac tissue recovery after myocardial infarction. Methods and Results: Using a preclinical mouse model of myocardial infarction, we demonstrate that a single intravenous bolus of n-apo AI (CSL111, 80 mg/kg) delivered immediately after reperfusion reduced the systemic and cardiac inflammatory response. N-apo AI treatment lowered the number of circulating leukocytes by 30±7% and their recruitment into the ischemic heart by 25±10% (all P <5.0×10 −2 ). This was associated with a reduction in plasma levels of the clinical biomarker of cardiac injury, cardiac troponin-I, by 52±17% ( P =1.01×10 −2 ). N-apo AI reduced the cardiac expression of chemokines that attract neutrophils and monocytes by 60% to 80% and lowered surface expression of integrin CD11b on monocytes by 20±5% (all P <5.0×10 −2 ). Fluorescently labeled n-apo AI entered the infarct and peri-infarct regions and colocalized with cardiomyocytes undergoing apoptosis and with leukocytes. We further demonstrate that n-apo AI binds to neutrophils and monocytes, with preferential binding to the proinflammatory monocyte subtype and partially via SR-BI (scavenger receptor BI). In patients with type 2 diabetes, we also observed that intravenous infusion of the same n-apo AI (CSL111, 80 mg/kg) similarly reduced the level of circulating leukocytes by 12±5% (all P <5.0×10 −2 ). Conclusions: A single intravenous bolus of n-apo AI delivered immediately post–myocardial infarction reduced the systemic and cardiac inflammatory response through direct actions on both the ischemic myocardium and leukocytes. These data highlight the anti-inflammatory effects of n-apo AI and provide preclinical support for investigation of its use for management of acute coronary syndromes in the setting of primary percutaneous coronary interventions.


2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
K. Kadner ◽  
S. Dobner ◽  
T. Franz ◽  
D. Bezuidenhout ◽  
M. Sirry ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document