Publications by authors named "Pianpian Huang"

Regulated in development and DNA damage response-1 (Redd1) is a stress-response gene that is transcriptionally induced by diverse stressful stimuli to influence cellular growth and survival. Although evidence suggests that aging may drive Redd1 expression in skeletal muscles, the expression patterns and functions of Redd1 in senescent cardiomyocytes remain unspecified. To address this issue, and models of cardiomyocyte senescence were established by administration of doxorubicin (Dox).

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The coronavirus disease 2019 (COVID-19) that occurred in Wuhan, Hubei Province, China, has been declared a public health emergency of international concern and a pandemic by the World Health Organization. The Chinese government has temporarily taken strong response measures and effective procedures to stop the further expansion and development of the epidemic. It is important for clinicians to screen, diagnose, and monitor COVID-19.

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The present study aimed to evaluate the value of serum amyloid A (SAA) in coronavirus disease 2019 (COVID-19) and compared the efficacy of SAA and C-reactive protein (CRP) in predicting the severity and recovery of COVID-19. A retrospective study was conducted on COVID-19 patients hospitalized in Wuhan No. 1 Hospital (Hubei, China) from January 21, 2020 to March 4, 2020.

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Senescence of cardiomyocytes is considered a key factor for the occurrence of doxorubicin (Dox)‑associated cardiomyopathy. The NOD‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome is reported to be involved in the process of cellular senescence. Furthermore, thioredoxin‑interactive protein (TXNIP) is required for NLRP3 inflammasome activation and is considered to be a key component in the regulation of the pathogenesis of senescence.

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Post‑infarction remodeling is accompanied and influenced by perturbations in the mammalian target of rapamycin (mTOR) signaling. Regulated in development and DNA damage response‑1 (Redd1) has been reported to be involved in DNA repair and modulation of mTOR activity. However, little is known about the role of Redd1 in the heart.

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