The fate and function of non-coding RNAs during necroptosis.

Necroptosis is a novel form of cell death which is activated when apoptotic cell death signals are disrupted. Accumulating body of observations suggests that noncoding RNAs, which are the lately discovered mystery of the human genome, are significantly associated with necroptotic signaling circuitry. The fate and function of miRNAs have been well documented in human disease, especially cancer. Recently, lncRNAs have gained much attention due to their diverse regulatory functions. Although available studies are currently based on bioinformatic analysis, predicted interactions desires further attention, as these hold significant promise and should not be overlooked. In the light of these, here we comprehensively review and discuss noncoding RNA molecules that play significant roles during execution of necroptotic cell death.

Necroptosis is a novel form of cell death triggered by disrupted apoptotic signals. noncoding RNAs, a mystery of the human genome, are significantly associated with necroptotic signaling. Their diverse regulatory functions, particularly in cancer, warrant further attention due to their potential.

Identification of non-coding RNA signatures in idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a deadly, chronic, progressive, irreversible interstitial lung disease characterized by the formation of scar tissue resulting in permanent lung damage. The average survival time following diagnosis is only 3-5 years, with a 5-year survival rate shorter than that of many cancers. Alveolar epithelial cell injury followed by irregular repair is the primary pathological process observed in patients with IPF. An evident characteristic of IPF is the development of fibroblastic foci representing active fibrotic areas. Most of the cells within these foci are believed to be myofibroblasts, which are thought to be the primary source of abnormal extracellular matrix production in IPF. The lung phenotype in IPF is characterized by significantly different processes from healthy lungs, including irregular apoptosis, oxidative stress, and epithelial-mesenchymal transition (EMT) pathways. AIMS: The exact cause of IPF is not fully understood and remains mysterious. It is not suppressing that non-coding RNAs are involved in the development and progression of IPF. Accordingly, here we aimed to identify non-coding RNA molecules during TGFß-induced myofibroblast activation. METHODS: Differential expression and functional enrichment analysis were employed to reveal the impact of non-coding RNAs during TGFß-associated lung fibrosis. RESULTS: Remarkably, LOC101448202, CZ1P-ASNS, LINC01503, IER3-AS1, MIR503HG, CLMAT3, LINC02593, ACTA2-AS1, LOC102723692, LOC107985728, and LOC105371064 were identified to be differentially altered during TGFß-stimulated myofibroblast activation. CONCLUSIONS: These findings strongly suggest that the mechanism of lung fibrosis is heavily under control of non-coding RNAs, and RNA-based therapies could be a promising approach for future therapeutic interventions to lung fibrosis.

MicroRNAs and cardiac fibrosis: A comprehensive update on mechanisms and consequences.

Fibrosis is a pathological wound-healing mechanism that results by the overactivation of fibroblasts. Fibrosis can become obstructive and deleterious during regeneration of various body tissues including cardiac muscle. This ultimately results in the development of cardiac fibrosis, characterized by an excessive buildup of extracellular matrix proteins. Thus, it could lead to arrhythmias and heart failure which creates a leading public health burden worldwide. MiRNAs are small non-coding RNAs with great potential for diagnostic and therapeutic purposes. Mounting evidence indicates that miRNAs are involved in the deregulation of tissue homeostasis during myocardial fibrosis. For instance, miRNAs that are implicated in the regulation of TGF-beta signaling pathway have been reported to be significantly altered in myocardial fibrosis. Accordingly, in this comprehensive review, we discuss and highlight recent available data on the role of miRNAs during myocardial fibrosis, providing valuable insights into the miRNA modulation of cardiac fibrosis and miRNAs targets that can be used in the future therapeutic interventions to cardiac fibrosis.

Radiologic and pathologic correlation of a renal venous hemangioma.

Renal hemangiomas, including the rare subtype of venous hemangioma, are typically non-cancerous, often asymptomatic, and usually discovered incidentally during imaging studies. Here, we report a unique case of a 59-year-old African-American female with a renal venous hemangioma that initially mimicked papillary-type renal cell carcinoma (RCC-pt) on imaging studies. The patient's presentation included a long history of rectal bleeding and an incidental discovery of a hypoattenuating mass in the left kidney during a contrast-enhanced CT scan. Renal MRI revealed a 3.5 cm left renal lower pole mass, presenting as heterogeneously hyperintense on T1-weighted images and hypointense on T2-weighted images, with gradual mild enhancement post-contrast. Subsequent total nephrectomy confirmed the histopathological diagnosis of a venous hemangioma. This case underlines the need for recognizing unique imaging features of renal venous hemangiomas, contributing to the differential diagnosis of T2 dark hypoenhancing renal masses. Correct interpretation may prevent unnecessary invasive procedures and operations, thereby improving patient management and outcomes.