Recent Insights Into Targeting Interleukin-27 in Coronary Artery Disease.

Coronary artery disease (CAD) is increasingly recognized as a chronic inflammatory condition. Interleukin-27 (IL-27), a cytokine from the IL-12 and IL-6 families, plays a dual role in CAD pathogenesis. It exacerbates disease by interacting with IL-1β and activating the NLRP3 inflammasome, promoting inflammation and tissue damage.

Aspirin for thromboembolism prophylaxis after fracture surgery.

Background: Venous thromboembolism poses a significant risk of fatal complications following fracture surgery. Clinical studies indicated that aspirin is prescribed in thromboprophylaxis but the efficacy and safety are not fully certain yet.

Methods: A meta-analysis was conducted to assess the safety and efficacy of aspirin in preventing thromboembolism prophylaxis in patients who have undergone fracture surgery.

Melatonin Inhibits ET-1 Production to Break Crosstalk Between Prostate Cancer and Bone Cells: Implication for Osteoblastic Bone Metastasis Treatment.

Bone metastasis is the primary cause of death among patients with advanced prostate cancer (PCa). PCa tends to spread to bones and acquire the bone-like phenotype, causing osteoblastic bone metastasis. Unfortunately, there is no effective treatment for this condition.

Immune landscape and regulatory mechanisms in human atherosclerotic coronary plaques: Evidence from single-cell and bulk transcriptomics.

Atherosclerosis is a chronic immuno-inflammatory disease, however, the immune landscape and regulatory mechanisms have not been clear. We detected seven principal immune cell clusters with distinct phenotypic and spatial characteristics using single-cell RNA-sequencing of aortic immune cells from patients with acute coronary syndrome and stable angina pectoris. Then we acquired 265 differentially expressed immune-related genes and the high scores were mainly found in T cells and monocytes, which were differentially regulated in atherosclerotic coronary plaques.

Soluble Guanylate Cyclase Activators and Stimulators in Patients with Heart Failure.

Purpose Of Review: This review sought to summarize the current emerging soluble guanylate cyclase activators and stimulators in patients with heart failure, both heart failure with reduced and preserved ejection fraction, to provide a reference for soluble guanylate cyclase activators and stimulators discovery.

Recent Findings: Heart failure is a common disease with considerable morbidity, hospitalization, and mortality Soluble guanylate cyclase is a key enzyme in the nitric oxide signaling pathway and has attracted rapidly growing interest as a therapeutic target in heart failure. Currently, several soluble guanylate cyclase agonists are in clinical development.

Melatonin Inhibits VEGF-Induced Endothelial Progenitor Cell Angiogenesis in Neovascular Age-Related Macular Degeneration.

Neovascular age-related macular degeneration (AMD) is described as abnormal angiogenesis in the retina and the leaking of fluid and blood that generates a huge, dark, blind spot in the center of the visual field, causing severe vision loss in over 90% of patients. Bone marrow-derived endothelial progenitor cells (EPCs) contribute to pathologic angiogenesis. Gene expression profiles downloaded from the eyeIntegration v1.

The ADAM9/WISP-1 axis cooperates with osteoblasts to stimulate primary prostate tumor growth and metastasis.

Metastatic prostate cancer (PCa) predicts a poor prognosis and lower likelihood of survival. Osteoblasts (OBs) are known to be responsible for the synthesis and mineralization of bone, although it is unclear as to whether PCa in the prostate gland cooperates with OBs in bone to promote PCa malignant transformation. We aimed to elucidate how primary PCa cells cooperate with distal OBs and contribute to the vicious cycle that leads to metastatic PCa.

Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α β expression.

Advanced prostate cancer often develops into bone metastasis, which is characterized by aberrant bone formation with chronic pain and lower chances of survival. No treatment exists as yet for osteoblastic bone metastasis in prostate cancer. The indolamine melatonin (N-acetyl-5-methoxytryptamine) is a major regulator of the circadian rhythm.

Melatonin interrupts osteoclast functioning and suppresses tumor-secreted RANKL expression: implications for bone metastases.

Cancer-related bone erosion occurs frequently in bone metastasis and is associated with severe complications such as chronic bone pain, fractures, and lower survival rates. In recognition of the fact that the darkness hormone melatonin is capable of regulating bone homeostasis, we explored its therapeutic potential in bone metastasis. We found that melatonin directly reduces osteoclast differentiation, bone resorption activity and promotes apoptosis of mature osteoclasts.

Melatonin impedes prostate cancer metastasis by suppressing MMP-13 expression.

Prostate cancer has high metastatic potential. Men with higher urinary levels of the sleep hormone melatonin are much less likely to develop advanced prostate cancer compared with men with lower levels of melatonin. Melatonin has shown anticancer activity in experimental investigations.

Prostate cancer-secreted CCN3 uses the GSK3β and β-catenin pathways to enhance osteogenic factor levels in osteoblasts.

Prostate cancer osteoblastic bone metastases are incurable and associated with chronic bone pain and a high mortality rate. Osteoclast-targeting drugs intended to prevent skeletal-related events associated with prostate cancer bone metastases do not prolong overall survival. Improved understanding of the bone-derived factors that contribute to prostate cancer osteoblastic bone metastases is required to design treatments that will improve morbidities and overall survival.

Thrombospondin 2 promotes tumor metastasis by inducing matrix metalloproteinase-13 production in lung cancer cells.

Thrombospondin (TSP)-2, a matricellular glycoprotein of the TSP family, regulates multiple biological functions, including proliferation, angiogenesis, cell adhesion, and extracellular matrix (ECM) modeling. The clinical relevance of TSP-2 has been explored in many different cancers. TSP-2 expression levels vary between different cancer types, and their role in tumor progression remains controversial.

Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression.

Background: Thrombospondin-2 (TSP-2) is a secreted matricellular glycoprotein that is found to mediate cell-to-extracellular matrix attachment and participates in many physiological and pathological processes. The expression profile of TSP-2 on tumors is controversial, and it up-regulates in some cancers, whereas it down-regulates in others, suggesting that the functional role of TSP-2 on tumors is still uncertain.

Methods: The expression of TSP-2 on prostate cancer progression was determined in the tissue array by the immunohistochemistry.