Local decorin delivery via hyaluronic acid microrods improves cardiac performance, ventricular remodeling after myocardial infarction

Mohindra, Priya; Zhong, Justin X.; Fang, Qizhi; Cuylear, Darnell L.; Huynh, Cindy; Qiu, Huiliang; Gao, Dongwei; Kharbikar, Bhushan N.; Huang, Xiao; Springer, Matthew L.; Lee, Randall J.; Desai, Tejal A.

doi:10.1038/s41536-023-00336-w

Cited by 5 publications

(2 citation statements)

References 87 publications

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“…Furthermore, novel pharmacotherapeutic approaches to improve adverse remodeling are currently being investigated. Intravenous administration of hyaluronan oligosaccharide and the use of human recombinant collagen III hydrogel both offer promising potential as therapeutics [27][28][29]. Also, a variety of other medications such as pirfenidone, angiotensin receptor blockers, or NLRP3 inflammasome inhibitors are currently evaluated in clinical trials [30].…”

Section: Discussionmentioning

confidence: 99%

Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction

Pec,

Buchner,

Fox

et al. 2024

Biomedicines

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Background: After acute myocardial infarction (AMI), inflammatory processes promote tissue remodeling at the infarct site. Procollagen III amino-terminal propeptide (PIIINP) is a circulating biomarker of type III collagen synthesis that has been shown to be associated with changes in left ventricular ejection fraction (LVEF) and predicts the occurrence of heart failure after AMI. We hypothesize that sleep-disordered breathing (SDB) promotes inflammation and myocardial fibrosis, leading to reduced myocardial salvage. Therefore, in patients with first-time AMI successfully treated with percutaneous coronary intervention (PCI), we aimed to investigate whether circulating levels of high-sensitivity C-reactive protein (hs-CRP) and PIIINP are elevated in patients with SDB compared to patients without SDB. Methods and Results: This cross-sectional analysis included a total of 88 eligible patients with first AMI and PCI pooled from two prospective studies and stratified according to the apnea–hypopnea index (AHI, with SDB: AHI ≥ 15 h−1). We analyzed circulating levels of hs-CRP and PIIINP 3–5 days after PCI. Patients with SDB had significantly higher levels of hs-CRP (18.3 mg/L [95% CI, 8.0–42.6] vs. 5.8 mg/L [95% CI, 4.2–19.8], p = 0.002) and PIIINP (0.49 U/mL [95% CI, 0.40–0.60] vs. 0.33 U/mL [95% CI, 0.28–0.43], p < 0.001). In a multivariable linear regression model accounting for important clinical confounders, SDB significantly predicted circulating levels of hs-CRP (p = 0.028). Similarly, only SDB was independently associated with PIIINP (p < 0.001). Only obstructive but not central AHI correlated with circulating levels of hs-CRP (p = 0.012) and PIIINP (p = 0.006) levels. Conclusions: The presence of obstructive SDB after AMI was independently associated with increased circulating levels of hs-CRP and PIIINP. Our results emphasize the important role of SDB as a common comorbidity and indicate increased inflammation and myocardial fibrosis in these patients.

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Section: Discussionmentioning

confidence: 99%

Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction

Pec,

Buchner,

Fox

et al. 2024

Biomedicines

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“…To evaluate the effect of the PAA/PASP only and HC-PILP on collagen fibrillogenesis, a collagen turbidity assay was performed following previous protocols 35 . Briefly, a 1 mg/ml stock solution of collagen type-I (Thermo Fischer Scientific, Waltham, MA, USA) was prepared by diluting high concentration collagen type-I with PBS and then subsequently kept on ice along with a 96-well plate.…”

Section: Collagen Turbidity Assaymentioning

confidence: 99%

Calcium phosphate nanoclusters modify periodontium remodeling and minimize orthodontic relapse

Cuylear,

Fu,

Chau

et al. 2024

Preprint

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Orthodontic relapse is one of the most prevalent concerns of orthodontic therapy. Relapse results in patients teeth reverting towards their pretreatment positions, which increases the susceptibility to functional problems, dental disease, and substantially increases the financial burden for retreatment. This phenomenon is thought to be induced by rapid remodeling of the periodontal ligament (PDL) in the early stages and poor bone quality in the later stages. Current therapies, including fixed or removable retainers and fiberotomies, have limitations with patient compliance and invasiveness. Approaches using biocompatible biomaterials, such as calcium phosphate polymer-induced liquid precursors (PILP), is an ideal translational approach for minimizing orthodontic relapse. Here, post-orthodontic relapse is reduced after a single injection of high concentration PILP (HC-PILP) nanoclusters by altering PDL remodeling in the early stage of relapse and improving trabecular bone quality in the later phase. HC-PILP nanoclusters are achieved by using high molecular weight poly aspartic acid (PASP, 14 kDa) and poly acrylic acid (PAA, 450 kDa), which resulted in a stable solution of high calcium and phosphate concentrations without premature precipitation. In vitro results show that HC-PILP nanoclusters prevented collagen type-I mineralization, which is essential for the tooth-periodontal ligament (PDL)-bone interphase. In vivo experiments show that the PILP nanoclusters minimize relapse and improve the trabecular bone quality in the late stages of relapse. Interestingly, HC-PILP nanoclusters also altered the remodeling of the PDL collagen during the early stages of relapse. Further in vitro experiments showed that HC-PILP nanoclusters alter the fibrillogenesis of collagen type-I by impacting the protein secondary structure. These findings propose a novel approach for treating orthodontic relapse and provide additional insight into the HC-PILP nanoclusters structure and properties on collagenous structure repair.

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Inflammation‐Targeted Nanomedicines Alleviate Oxidative Stress and Reprogram Macrophages Polarization for Myocardial Infarction Treatment

Hu,

Li,

et al. 2024

Advanced Science

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Myocardial infarction (MI) is a critical global health challenge, with current treatments limited by the complex MI microenvironment, particularly the excessive oxidative stress and intense inflammatory responses that exacerbate cardiac dysfunction and MI progression. Herein, a mannan‐based nanomedicine, Que@MOF/Man, is developed to target the inflammatory infarcted heart and deliver the antioxidative and anti‐inflammatory agent quercetin (Que), thereby facilitating a beneficial myocardial microenvironment for cardiac repair. The presence of mannan on the nanoparticle surface enables selective internalization by macrophages rather than cardiomyocytes. Que@MOF/Man effectively neutralizes reactive oxygen species in macrophages to reduce oxidative stress and promote their differentiation into a reparative phenotype, reconciling the inflammatory response and enhancing cardiomyocyte survival through intercellular communication. Owing to the recruitment of macrophages into inflamed myocardium post‐MI, in vivo, administration of Que@MOF/Man in MI rats revealed the specific distribution into the injured myocardium compared to free Que. Furthermore, Que@MOF/Man exhibited favorable results in resolving inflammation and protecting cardiomyocytes, thereby preventing further myocardial remodeling and improving cardiac function in MI rats. These findings collectively validate the rational design of an inflammation‐targeted delivery strategy to mitigate oxidative stress and modulate the inflammation response in the injured heart, presenting a therapeutic avenue for MI treatment.

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Local decorin delivery via hyaluronic acid microrods improves cardiac performance, ventricular remodeling after myocardial infarction

Cited by 5 publications

References 87 publications

Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction

Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction

Calcium phosphate nanoclusters modify periodontium remodeling and minimize orthodontic relapse

Inflammation‐Targeted Nanomedicines Alleviate Oxidative Stress and Reprogram Macrophages Polarization for Myocardial Infarction Treatment

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