Pathobiology of cardiovascular diseases: an update

Buja, L. M.; Ottaviani, Giulia; Mitchell, Richard N.

doi:10.1016/j.carpath.2019.06.002

Cited by 34 publications

(28 citation statements)

References 181 publications

(230 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Altered endothelial cell morphology resulting from external stress has been reported to be capable of inducing intrinsic pathway-mediated defense mechanisms to avoid cell death [42]. Therefore, it is considered to be a key event involved in the development and progression of many cardiovascular diseases, including hypertension, atherosclerosis, and type II diabetes [2,3,26]. Apoptosis, well known as programmed cell death or cellular suicide, can lead to activation of caspases and induce the human inflammatory diseases and cardiovascular dysfunction [43].…”

Section: T-bhp Induces Apoptosis Necrosis and Inflammatory Induced mentioning

confidence: 99%

“…Aortic endothelial cells (ECs) are well known for their abilities to maintain homeostasis and hemostasis in the human cardiovascular system. Increased evidence suggested that endothelial dysfunction is involved in the initiation and progression of many cardiovascular diseases (CVDs) [1][2][3]. The endothelial cells, which form a single continuous layer of blood vessels, are a distinctive target for cytotoxic or cytostatic effects induced by systemic oxidative stress and inflammatory imbalance [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

Yeh

Liu²,

Lai³

2020

Int. J. Med. Sci.

View full text Add to dashboard Cite

Background: Endothelial dysfunction is one of the underlying causes for vascular diseases. tert-Butyl hydroperoxide (t-BHP), a short-chain lipid hydroperoxide analog, has been reported to cause adverse effects in different systems. However, the adverse actions of t-BHP on inducing endothelial dysfunction are unclear and remain under investigation. Aim of the present study was to identify the pathobiological mechanisms of t-BHP in rat aortic endothelial cells and thoracic aorta. Methods: Primary cultured cells were treated with vehicle or t-BHP (50, 100, 250, 500, and 1,000 µM). Cells were harvested and specific analyses regarding cellular apoptosis, necrosis, and senescence were conducted. Additionally, t-BHP (0.1, 0.2, and 0.4 mmol/kg body weight) or vehicle were administered to male rats (the young group at 6 weeks of age and the mature adult group at 24 weeks of age) daily through intraperitoneal injections. At 10 days after the first drug treatment apoptotic endothelial toxicity was evaluated by biochemical, histological, and immunofluorescent staining analyses. Results: Dose-dependent effects of t-BHP were observed for the reduction of cell viability, deterioration of cell toxicity, initiation of cell cycle arrest, and triggering of apoptosis and necrosis. Moreover, increase of cells stained positive for senescence-associated beta-galactosidase (SA-β-Gal), amelioration of telomerase activity, and precipitations of necrotic, cell cycle, and apoptotic signaling regulatory proteins were also found in the in vitro model. In the in vivo study, results indicated that t-BHP at higher doses enlarged the intima-medial thickness of descending aorta in the mature adult group, but led to aortic narrowing in the young group. Increased injuries were observed by upregulating endothelial apoptosis-and senescence-positive staining, along with caspase-3 activity and down-regulating telomerase activity. Conclusion: These results confirmed that t-BHP impaired aortic endothelial cell survival at least partially by the activation of p53-mediated signaling pathways, inhibition of cell cycle regulatory proteins, and initiation of cellular senescence-related signaling pathways. In conclusion, t-BHP was found to be a major trigger for impairing aortic endothelial cell survival and deteriorating vascular dysfunction in experimental practice.

show abstract

Section: T-bhp Induces Apoptosis Necrosis and Inflammatory Induced mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

Yeh

Liu²,

Lai³

2020

Int. J. Med. Sci.

View full text Add to dashboard Cite

show abstract

“…In the 20th and 21st centuries, autopsy pathology has continued to be primarily responsible for the discovery or elucidation of the pathogenesis of new diseases, such as acquired immunodeficiency syndrome due to human immunodeficiency virus, as well as documentation of effects of new therapies. [138][139][140][141] Both the discovery process as well as diagnostic pathology have been enhanced by the coupling of gross examination and light microscopy with new techniques, including electron microscopy, fluorescence microscopy, histochemistry, and immunohistochemistry. From the 1970s onward, immunocytochemistry has become a powerful and ubiquitous component of diagnostic pathology.…”

Section: Impact Of Scientific Advances On Pathologymentioning

confidence: 99%

“…Application of nextgeneration sequencing to formalin-fixed paraffin-embedded tissues also has become feasible, with great potential for a renaissance of genomic research on human tissues, including an expanded role for the autopsy ("molecular autopsy"). [139][140][141] Pathologists have taken on the key role of stewards of human tissue specimens for diagnosis and research into the future. 165 Applications of health informatics technology are making increasingly prevalent telecommunications between physicians and scientists and between professionals and patients and subject participants.…”

Section: Impact Of Scientific Advances On Pathologymentioning

confidence: 99%

The Texas Society of Pathologists: molded by the legacy of pathology and focused on excellence in medicine for 100 years and beyond

Buja

2020

Baylor University Medical Center Proceedings

Self Cite

View full text Add to dashboard Cite

In 1921, 16 Texas pathologists gathered in Dallas, Texas, to found the Texas Society of Pathologists (TSP). The TSP is now the oldest state pathology society in the USA with continuity traced back to its founding 100 years ago. This article aims to both commemorate the TSP centennial and to provide context for the remarkable success of the society. The article takes a look back and a look forward from 1921. The look back focuses on the development of the field of pathology and the maturation of medicine and pathology in the USA and Texas. The look forward encompasses developments in science, technology, American health care policy, and medicine that have impacted Texas pathologists and influenced proactive initiatives of the TSP. The review of the life and times of the TSP highlights the importance of leaders and leadership in shaping outcomes. Complexities and uncertainties of the contemporary health care scene point to the need for continued strong leadership. The successful past century and hopeful future of the TSP are inextricably linked to the guiding principle of the TSP, which is a focus on continual striving for excellence in medicine. KEYWORDS Health care policy; history; Texas society of pathologists "I have great respect for the past. If you don't know where you've come from, you don't know where you are going."-Maya Angelou (1928-2014) "Of necessity an historical account must be largely biographical. Men and their books have built pathology. Yet without a point of view which takes account of the major social movements of general history, no real conception of the historical development of any subject is possible."-Esmond R. Long, MD (1890-1979) "If I have seen further than others, it is by standing upon the shoulders of giants."-Isaac Newton (1642-1726)

show abstract

“…Even if manifestations such as an episode of heart failure decompensation give time to seek medical help and are manageable, SCD leaves no room for reaction. SCD can be divided into two major categories-deaths that occur as a consequence of a mechanical complication, for instance, myocardial rupture or left ventricular outflow tract obstruction in HCM and deaths that have a malignant arrhythmic origin [4]. The latter cases are more likely to have an autopsy negative SCD since the post-mortem analysis of the cardiac conduction system is not routinely feasible given that it is technically demanding [5].…”

Section: Introductionmentioning

confidence: 99%

Updating the Risk Stratification for Sudden Cardiac Death in Cardiomyopathies: The Evolving Role of Cardiac Magnetic Resonance Imaging. An Approach for the Electrophysiologist

et al. 2020

View full text Add to dashboard Cite

The prevention of sudden cardiac death (SCD) in cardiomyopathies (CM) remains a challenge. The current guidelines still favor the implantation of devices for the primary prevention of SCD only in patients with severely reduced left ventricular ejection fraction (LVEF) and heart failure (HF) symptoms. The implantation of an implantable cardioverter-defibrillator (ICD) is a protective barrier against arrhythmic events in CMs, but the benefit does not outweigh the cost in low risk patients. The identification of high risk patients is the key to an individualized prevention strategy. Cardiac magnetic resonance (CMR) provides reliable and reproducible information about biventricular function and tissue characterization. Furthermore, late gadolinium enhancement (LGE) quantification and pattern of distribution, as well as abnormal T1 mapping and extracellular volume (ECV), representing indices of diffuse fibrosis, can enhance our ability to detect high risk patients. CMR can also complement electro-anatomical mapping (EAM), a technique already applied in the risk evaluation and in the ventricular arrhythmias ablation therapy of CM patients, providing a more accurate assessment of fibrosis and arrhythmic corridors. As a result, CMR provides a new insight into the pathological substrate of CM. CMR may help identify high risk CM patients and, combined with EAM, can provide an integrated evaluation of scar and arrhythmic corridors in the ablative therapy of ventricular arrhythmias.

show abstract

Pathobiology of cardiovascular diseases: an update

Cited by 34 publications

References 181 publications

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

The Texas Society of Pathologists: molded by the legacy of pathology and focused on excellence in medicine for 100 years and beyond

Updating the Risk Stratification for Sudden Cardiac Death in Cardiomyopathies: The Evolving Role of Cardiac Magnetic Resonance Imaging. An Approach for the Electrophysiologist

Contact Info

Product

Resources

About