Pheochromocytoma: A review of the literature

Watkins, Dale B.

doi:10.1016/0021-9681(57)90041-3

Cited by 32 publications

(1 citation statement)

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“…Cardiac injury has long been observed in diseases associated with catecholamine surges. As highlighted by Watkins in a review article published in 1957 ( 14 ), myocardial fibrosis and inflammatory responses were observed in patients suffering from pheochromocytoma, a rare but treacherous catecholamine-producing tumor. More than a century ago, intravenous injections of adrenalin were shown to induce myocarditis and the morphological features of cardiomyocyte degeneration and necrosis in rabbits ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

Catecholamine Surges Cause Cardiomyocyte Necroptosis via a RIPK1–RIPK3-Dependent Pathway in Mice

Cai

Liu

et al. 2021

Front. Cardiovasc. Med.

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Background: Catecholamine surges and resultant excessive β-adrenergic stimulation occur in a broad spectrum of diseases. Excessive β-adrenergic stimulation causes cardiomyocyte necrosis, but the underlying mechanism remains obscure. Necroptosis, a major form of regulated necrosis mediated by RIPK3-centered pathways, is implicated in heart failure; however, it remains unknown whether excessive β-adrenergic stimulation-induced cardiac injury involves necroptosis. Hence, we conducted the present study to address these critical gaps.Methods and Results: Two consecutive daily injections of isoproterenol (ISO; 85 mg/kg, s.c.) or saline were administered to adult mixed-sex mice. At 24 h after the second ISO injection, cardiac area with Evans blue dye (EBD) uptake and myocardial protein levels of CD45, RIPK1, Ser166-phosphorylated RIPK1, RIPK3, and Ser345-phosphorylated MLKL (p-MLKL) were significantly greater, while Ser321-phosphorylated RIPK1 was significantly lower, in the ISO-treated than in saline-treated wild-type (WT) mice. The ISO-induced increase of EBD uptake was markedly less in RIPK3−/− mice compared with WT mice (p = 0.016). Pretreatment with the RIPK1-selective inhibitor necrostatin-1 diminished ISO-induced increases in RIPK3 and p-MLKL in WT mice and significantly attenuated ISO-induced increases of EBD uptake in WT but not RIPK3−/− mice.Conclusions: A large proportion of cardiomyocyte necrosis induced by excessive β-adrenergic stimulation belongs to necroptosis and is mediated by a RIPK1–RIPK3-dependent pathway, identifying RIPK1 and RIPK3 as potential therapeutic targets for catecholamine surges.

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Section: Introductionmentioning

confidence: 99%