Publications by authors named "Yu-Lin Bao"

Background: Mitochondrial dysfunction is linked to myocardial ischemia-reperfusion (I/R) injury. Checkpoint kinase 1 (CHK1) could facilitate cardiomyocyte proliferation, however, its role on mitochondrial function in I/R injury remains unknown.

Methods: To investigate the role of CHK1 on mitochondrial function following I/R injury, cardiomyocyte-specific knockout/overexpression mouse models were generated.

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  • Circular RNAs (circRNAs), particularly circIGF1R, are identified as crucial for cardiac regeneration and show potential as biomarkers and therapeutic targets in heart disease.
  • circIGF1R expression is higher in neonatal hearts but decreases with maturation; it is up-regulated after cardiac injury and linked to improved outcomes in patients with acute myocardial infarction.
  • Mechanistically, circIGF1R promotes heart cell proliferation and reduces heart damage by interacting with DDX5, triggering the β-catenin signaling pathway, which enhances levels of growth-related proteins cyclin D1 and c-Myc.
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  • The peroxisome is an organelle that plays a key role in various metabolic functions, and PEX3 is a crucial regulator of these processes.
  • Researchers found that knocking out PEX3 specifically in heart cells (Pex3-KO) leads to an imbalance in redox homeostasis and disrupts heart cell growth and development.
  • The study suggests that PEX3 aids in heart repair by affecting plasmalogen metabolism and influencing the AKT/GSK3β signaling pathway, indicating it could be an innovative target for therapies aimed at repairing heart damage.
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  • CHK1-targeted cancer therapies can increase the risk of heart problems, especially when combined with gemcitabine, but the exact reasons for this are not well understood.
  • The study used human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and mouse models to investigate the cardiotoxic effects caused by these treatments, finding that they led to mitochondrial damage and heart dysfunction.
  • The research highlighted the importance of mitochondrial CHK1, which helps maintain mitochondrial function, and suggested that boosting levels of SIRT3 could be a promising strategy to protect against heart damage related to these cancer therapies.
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Colchicine has demonstrated promising effects in inhibiting local and systemic inflammation during acute coronary syndrome (ACS). However, the efficacy of colchicine in ACS is controversial. We performed a meta-analysis to assess the utility of colchicine in ACS by systematically searching randomized controlled trials.

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