Editorial: Insights in cardiovascular therapeutics: 2021 – cell death, cardiovascular injuries, and novel targets of cardiovascular therapeutics
Genre
Article (Other)Date
2022-07-26Author
XU, KEMAN
Khan, Mohsin
Yu, Jun
Snyder, Nathaniel
Wu, Sheng
Vazquez-Padron, Roberto I.
Wang, Hong
Yang, Xiaofeng
Group
Cardiovascular Research Center (Temple University)Centers for Metabolic Disease Research (Temple University)
Department
Cardiovascular SciencesBiomedical Education and Data Sciences
Permanent link to this record
http://hdl.handle.net/20.500.12613/8268Metadata
Show full item recordDOI
https://doi.org/10.3389/fcvm.2022.981544Abstract
With the effort and support of the authors, editorial office, and editorial team, the Frontiers in Cardiovascular Medicine, Cardiovascular Therapeutics Section-Research Topic “Insights in Cardiovascular Therapeutics: 2021” has achieved great success and is attracting interest from the cardiovascular community. Here, we spotlight 12 studies published in our section that related to cell death and cardiovascular injuries, as well as some recent advances in the field that have tremendous potential in cardiovascular therapy. In addition, these highlights may serve as the foundation for some new developments in our Cardiovascular Therapeutics areas. In 2022, we will keep working to create a fantastic platform for cardiologists, translational cardiovascular scientists, and cardiovascular pharmacological scientists to share new results and data in clinical cardiology and translational cardiovascular therapeutics.Citation
Xu K, Khan M, Yu J, Snyder NW, Wu S, Vazquez-Padron RI, Wang H and Yang X (2022) Editorial: Insights in cardiovascular therapeutics: 2021 – cell death, cardiovascular injuries, and novel targets of cardiovascular therapeutics. Front. Cardiovasc. Med. 9:981544. doi: 10.3389/fcvm.2022.981544Citation to related work
Frontiers MediaHas part
Frontiers in Cardiovascular Medicine, Vol. 9ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.eduScopus Count
Collections
Except where otherwise noted, this item's license is described as Attribution CC BY
Related items
Showing items related by title, author, creator and subject.
-
Association of Changes in Cardiovascular Health Metrics and Risk of Subsequent Cardiovascular Disease and MortalityBackground The extent to which change in cardiovascular health (CVH) in midlife reduces risk of subsequent cardiovascular disease and mortality is unclear. Methods and Results CVH was computed at 2 ARIC (Atherosclerosis Risk in Communities) study visits in 1987 to 1989 and 1993 to 1995, using 7 metrics (smoking, body mass index, total cholesterol, blood glucose, blood pressure, physical activity, and diet), each classified as poor, intermediate, and ideal. Overall CVH was classified as poor, intermediate, and ideal to correspond to 0 to 2, 3 to 4, and 5 to 7 metrics at ideal levels. There 10 038 participants, aged 44 to 66 years that were eligible. From the first to the second study visit, there was an improvement in overall CVH for 17% of participants and a decrease in CVH for 21% of participants. At both study visits, 28%, 27%, and 6% had poor, intermediate, and ideal overall CVH, respectively. Compared with those with poor CVH at both visits, the risk of cardiovascular disease (hazard ratio [HR], 0.26; 95% CI, 0.20-0.34) and mortality (HR, 0.35; 95% CI, 0.29-0.44) was lowest in those with ideal CVH at both measures. Improvement from poor to intermediate/ideal CVH was also associated with a lower risk of cardiovascular disease (HR, 0.67; 95% CI, 0.59-0.75) and mortality (HR, 0.80; 95% CI, 0.72-0.89). Conclusions Improvement in CVH or stable ideal CVH, compared with those with poor CVH over time, is associated with a lower risk of incident cardiovascular disease and all-cause mortality. The change in smoking status and cholesterol may have accounted for a large part of the observed association.
-
SARS-CoV-2, ACE2, and Hydroxychloroquine: Cardiovascular Complications, Therapeutics, and Clinical Readouts in the Current SettingsThe rapidly evolving coronavirus disease 2019 (COVID-19, caused by severe acute respiratory syndrome coronavirus 2- SARS-CoV-2), has greatly burdened the global healthcare system and led it into crisis in several countries. Lack of targeted therapeutics led to the idea of repurposing broad-spectrum drugs for viral intervention. In vitro analyses of hydroxychloroquine (HCQ)’s anecdotal benefits prompted its widespread clinical repurposing globally. Reports of emerging cardiovascular complications due to its clinical prescription are revealing the crucial role of angiotensin-converting enzyme 2 (ACE2), which serves as a target receptor for SARS-CoV-2. In the present settings, a clear understanding of these targets, their functional aspects and physiological impact on cardiovascular function are critical. In an up-to-date format, we shed light on HCQ’s anecdotal function in stalling SARS-CoV-2 replication and immunomodulatory activities. While starting with the crucial role of ACE2, we here discuss the impact of HCQ on systemic cardiovascular function, its associated risks, and the scope of HCQ-based regimes in current clinical settings. Citing the extent of HCQ efficacy, the key considerations and recommendations for the use of HCQ in clinics are further discussed. Taken together, this review provides crucial insights into the role of ACE2 in SARS-CoV-2-led cardiovascular activity, and concurrently assesses the efficacy of HCQ in contemporary clinical settings.
-
OWNER OF A BROKEN HEART: STEM CELL THERAPY, INFLAMMATION, AND WOUND HEALING IN THE INFARCTED HEARTAcute damage to the heart, as in the case of myocardial infarction (MI), triggers a robust inflammatory response to the sterile injury and requires a complex and highly organized wound healing processes for survival. Cortical bone stem cell (CBSC) therapy has been shown to attenuate the decline in cardiac function associated with MI in both mouse and swine models. However, the cellular changes brought about by CBSC treatment and their relationship to inflammation and the wound healing process are unknown. We observed that CBSCs secrete paracrine factors known to have immunomodulatory properties, most notably Macrophage Colony Stimulating Factor (M-CSF) and Transforming Growth Factor-b, but not IL-4. Macrophages treated with CBSC medium containing these factors polarized to a hybrid M2a/M2c phenotype characterized by increased CD206 expression but not CD206 and CD163 co-expression, increased efferocytic ability, increased IL-10, TGF-b and IL-1RA secretion, and increased mitochondrial respiration in the absence of IL-4. Media from these macrophages increased proliferation and decreased a-Smooth Muscle Actin expression in fibroblasts in vitro. In addition, CBSC therapy increased macrophages, CD4+ T-cells, and fibroblasts while decreasing myocyte, macrophage, and total apoptosis in an in vivo swine model of MI. From these data, we conclude that CBSCs are modulating the immune response to MI in favor of an anti-inflammatory reparative response, ultimately reducing cell death and altering fibroblast populations resulting in smaller scar and preserved cardiac geometry and function.
