Pericardial fluid: an underrated molecular library of heart conditions and a potential vehicle for cardiac therapy

Trindade, Fábio; Vitorino, Rui; Leite‐Moreira, Adelino F.; Falcão-Pires, Inês

doi:10.1007/s00395-019-0716-3

Cited by 40 publications

(29 citation statements)

References 175 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that MAO-A activity is enhanced by I/R injury and is responsible for the precipitation of hydrogen peroxide and the progression towards left ventricle hypertrophy and cardiac remodeling [93]. Increased influx of mitochondrial iron stimulates the formation of more potent and deleterious hydroxyl radical groups from hydrogen peroxide [94,95]. Although the continuous release of ROS from mitochondria during normal conditions appears to play a necessary role in the maintenance of basal cellular function, transiently elevated ROS levels can promote selective protein synthesis, preconditioning, and changes in vascular tone [96,97].…”

Section: Mitochondrial Oxidative Stressmentioning

confidence: 99%

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Zhou

Toan

2020

Biomolecules

View full text Add to dashboard Cite

Mitochondria are key regulators of cell fate through controlling ATP generation and releasing pro-apoptotic factors. Cardiac ischemia/reperfusion (I/R) injury to the coronary microcirculation has manifestations ranging in severity from reversible edema to interstitial hemorrhage. A number of mechanisms have been proposed to explain the cardiac microvascular I/R injury including edema, impaired vasomotion, coronary microembolization, and capillary destruction. In contrast to their role in cell types with higher energy demands, mitochondria in endothelial cells primarily function in signaling cellular responses to environmental cues. It is clear that abnormal mitochondrial signatures, including mitochondrial oxidative stress, mitochondrial fission, mitochondrial fusion, and mitophagy, play a substantial role in endothelial cell function. While the pathogenic role of each of these mitochondrial alterations in the endothelial cells I/R injury remains complex, profiling of mitochondrial oxidative stress and mitochondrial dynamics in endothelial cell dysfunction may offer promising potential targets in the search for novel diagnostics and therapeutics in cardiac microvascular I/R injury. The objective of this review is to discuss the role of mitochondrial oxidative stress on cardiac microvascular endothelial cells dysfunction. Mitochondrial dynamics, including mitochondrial fission and fusion, are critically discussed to understand their roles in endothelial cell survival. Finally, mitophagy, as a degradative mechanism for damaged mitochondria, is summarized to figure out its contribution to the progression of microvascular I/R injury.

show abstract

Section: Mitochondrial Oxidative Stressmentioning

confidence: 99%

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Zhou

Toan

2020

Biomolecules

View full text Add to dashboard Cite

show abstract

“…In addition to blood, CSF, and urine, sMAC is found in synovial, pleural, pericardial and peritoneal fluid under conditions of infection, malignancy, or autoimmune disease (listed in Table 4). These fluids are routinely collected for diagnostic purposes, primarily to identify bacterial or viral infections, as well as other medical conditions (196)(197)(198)(199)(200)(201). Less commonly analyzed is blister fluid from burn patients.…”

Section: Synovial and Mucosal Fluidsmentioning

confidence: 99%

Soluble Membrane Attack Complex: Biochemistry and Immunobiology

2020

View full text Add to dashboard Cite

“…After 22 h, cells were replenished with fresh growth medium (Wolint et al, 2019), then 2 h later, cells were transfected with siRNA. Twenty-four hours after transfection, cell viability was measured through MTT assay as previously described (Trindade et al, 2019).…”

Section: Cell Survival Assaymentioning

confidence: 99%

Resveratrol Improves Bnip3-Related Mitophagy and Attenuates High-Fat-Induced Endothelial Dysfunction

Tan

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Statin treatment reduces cardiovascular risk. However, individuals with well-controlled low-density lipoprotein (LDL) levels may remain at increased risk owing to persistent high triglycerides and low high-density lipoprotein cholesterol. Because resveratrol promotes glucose metabolism and mitigates cardiovascular disorders, we explored its mechanism of protective action on high-fat-induced endothelial dysfunction. Human umbilical venous endothelial cells were treated with oxidized LDL (ox-LDL) in vitro. Endothelial function, cell survival, proliferation, migration, and oxidative stress were analyzed through western blots, quantitative polymerase chain reaction, ELISA, and immunofluorescence. ox-LDL induced endothelial cell apoptosis, proliferation arrest, and mobilization inhibition, all of which resveratrol reduced. ox-LDL suppressed the activities of mitochondrial respiration complex I and III and reduced levels of intracellular antioxidative enzymes, resulting in reactive oxygen species overproduction and mitochondrial dysfunction. Resveratrol treatment upregulated Bnip3-related mitophagy and prevented ox-LDL-mediated mitochondrial respiration complexes inactivation, sustaining mitochondrial membrane potential and favoring endothelial cell survival. We found that resveratrol enhanced Bnip3 transcription through hypoxia-inducible factor 1 (HIF1) and 5 AMP-activated protein kinase (AMPK). Inhibition of AMPK and HIF1 abolished resveratrol-mediated protection of mitochondrial redox balance and endothelial viability. Together, these data demonstrate resveratrol reduces hyperlipemiarelated endothelial damage by preserving mitochondrial homeostasis.

show abstract

Pericardial fluid: an underrated molecular library of heart conditions and a potential vehicle for cardiac therapy

Cited by 40 publications

References 175 publications

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Soluble Membrane Attack Complex: Biochemistry and Immunobiology

Resveratrol Improves Bnip3-Related Mitophagy and Attenuates High-Fat-Induced Endothelial Dysfunction

Contact Info

Product

Resources

About