Therapies to prevent post-infarction remodelling: From repair to regeneration

Contessotto, Paolo; Pandit, Abhay

doi:10.1016/j.biomaterials.2021.120906

Cited by 35 publications

(28 citation statements)

References 178 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The pathophysiological response to ischemic injury mainly includes three different but overlapping processes, namely, inflammation, proliferation, and remodeling. [10][11][12] Myocardial ischemia can cause cardiomyocyte damage; if the duration of ischemia is prolonged, it causes cardiomyocyte death, triggering the release of potent proinflammatory signals which induce the degradation of extracellular matrix (ECM) and dysfunction of normal cells. [13] The damaged myocardium secretes damage-related molecular patterns (DAMPs) to recruit inflammatory cell populations that mediate the successive phase of remodeling after ischemia.…”

Section: Introductionmentioning

confidence: 99%

Engineering Injectable Anti‐Inflammatory Hydrogels to Treat Acute Myocardial Infarction

Zhang

Liu

2022

Advanced NanoBiomed Research

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) poses serious threats to human health. Suppressing long-term inflammation is a promising strategy to improve cardiac function following AMI. However, the direct injection of anti-inflammatory drugs after AMI can trigger adverse events due to systemic off-target effects and bioavailability issues. Injectable hydrogels can be used for local transportation of various therapeutic molecules through minimally invasive technology to overcome the side effects of intravenous injection. Herein, the anti-inflammatory mechanisms and applications of injectable hydrogels are reviewed to deliver antiinflammatory drugs, antioxidants, immune-regulation drugs, stem cells and their derived exosomes, and therapeutic gas to reduce the inflammatory response to treat AMI. The outlook on challenges in the design of hydrogels for treating AMI is also presented.

show abstract

Section: Introductionmentioning

confidence: 99%

Engineering Injectable Anti‐Inflammatory Hydrogels to Treat Acute Myocardial Infarction

Zhang

Liu

2022

Advanced NanoBiomed Research

View full text Add to dashboard Cite

show abstract

“…We acknowledge that HFrEF and HFpEF have distinct clinical manifestations in humans, and that animal models do not entirely replicate those features [ 9 , 10 ]. Although we recognize this limitation, we believe they might be effective in understanding more about the metabolic changes associated with HF.…”

Section: Introductionmentioning

confidence: 99%

Understanding How Heart Metabolic Derangement Shows Differential Stage Specificity for Heart Failure with Preserved and Reduced Ejection Fraction

2022

Self Cite

View full text Add to dashboard Cite

Heart failure (HF) is a clinical condition defined by structural and functional abnormalities in the heart that gradually result in reduced cardiac output (HFrEF) and/or increased cardiac pressures at rest and under stress (HFpEF). The presence of asymptomatic individuals hampers HF identification, resulting in delays in recognizing patients until heart dysfunction is manifested, thus increasing the chance of poor prognosis. Given the recent advances in metabolomics, in this review we dissect the main alterations occurring in the metabolic pathways behind the decrease in cardiac function caused by HF. Indeed, relevant preclinical and clinical research has been conducted on the metabolite connections and differences between HFpEF and HFrEF. Despite these promising results, it is crucial to note that, in addition to identifying single markers and reliable threshold levels within the healthy population, the introduction of composite panels would strongly help in the identification of those individuals with an increased HF risk. That said, additional research in the field is required to overcome the current drawbacks and shed light on the pathophysiological changes that lead to HF. Finally, greater collaborative data sharing, as well as standardization of procedures and approaches, would enhance this research field to fulfil its potential.

show abstract

“…When in vivo transplanted or injected MSC are exposed to an ischemic environment, the nutritional restriction and low oxygen content significantly lower their lifespan, via apoptotic processes [ 7 ], and their therapeutic potential [ 5 , 8 , 9 , 10 ]. Because of their low viability after transplantation, it is currently assumed that the favorable benefits of MSC, such as enhanced angiogenesis, inflammation suppression and immune-modulation, are primarily due to released trophic factors and to EVs, or linked to apoptotic processes [ 7 , 11 ], rather than their direct regenerative capabilities [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the concept of priming cells by preconditioning them to promote quiescence is gaining popularity as a way to improve the anti-inflammatory, regenerative and survival rates of MSC in vivo [ 5 , 10 , 11 , 17 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Regenerative and Anti-Inflammatory Potential of Regularly Fed, Starved Cells and Extracellular Vesicles In Vivo

Ferro

Spelat

Shaw

et al. 2022

Cells

Self Cite

View full text Add to dashboard Cite

Background: Mesenchymal stem/stromal cells (MSC) have been employed successfully in immunotherapy and regenerative medicine, but their therapeutic potential is reduced considerably by the ischemic environment that exists after transplantation. The assumption that preconditioning MSC to promote quiescence may result in increased survival and regenerative potential upon transplantation is gaining popularity. Methods: The purpose of this work was to evaluate the anti-inflammatory and regenerative effects of human bone marrow MSC (hBM-MSC) and their extracellular vesicles (EVs) grown and isolated in a serum-free medium, as compared to starved hBM-MSC (preconditioned) in streptozotocin-induced diabetic fractured male C57BL/6J mice. Results: Blood samples taken four hours and five days after injection revealed that cells, whether starved or not, generated similar plasma levels of inflammatory-related cytokines but lower levels than animals treated with EVs. Nonetheless, starved cells prompted the highest production of IL-17, IL-6, IL-13, eotaxin and keratinocyte-derived chemokines and induced an earlier soft callus formation and mineralization of the fracture site compared to EVs and regularly fed cells five days after administration. Conclusions: Preconditioning may be crucial for refining and defining new criteria for future MSC therapies. Additionally, the elucidation of mechanisms underpinning an MSC’s survival/adaptive processes may result in increased cell survival and enhanced therapeutic efficacy following transplantation.

show abstract

Therapies to prevent post-infarction remodelling: From repair to regeneration

Cited by 35 publications

References 178 publications

Engineering Injectable Anti‐Inflammatory Hydrogels to Treat Acute Myocardial Infarction

Engineering Injectable Anti‐Inflammatory Hydrogels to Treat Acute Myocardial Infarction

Understanding How Heart Metabolic Derangement Shows Differential Stage Specificity for Heart Failure with Preserved and Reduced Ejection Fraction

Regenerative and Anti-Inflammatory Potential of Regularly Fed, Starved Cells and Extracellular Vesicles In Vivo

Contact Info

Product

Resources

About