Short-term aromatase inhibition induces prostatic alterations in adult wistar rat: A biochemical, histopathological and immunohistochemical study

Synthesis, In Silico, and Biological Evaluation of a Borinic Tryptophan-Derivative That Induces Melatonin-like Amelioration of Cognitive Deficit in Male Rat

“…There were significant differences between the control and gonadectomized groups in all measured immunohistochemistry assays ( Figure 10 and Figure 11 , F ≥ 11.28, p < 0.01). In fact, the gonadectomy and the consequent hormonal deprivation reduced neuronal survival and increased the tissue changes associated with amyloid presence, as has been reported [ 51 , 52 , 53 ].…”

Understanding human aging and the fundamental cell signaling link in age-related diseases: the middle-aging hypovascularity hypoxia hypothesis

“…Loss of micro-vascularity ( Hofer and Morey, 2018 ; Gerbie et al, 2021 ) implies an important role for cyclic/chronic hypoxic milieu ( Fine and Norman, 2008 ) in regionalizing perfusion and contributing to the progression of age-related degenerative comorbid diseases in humans. Age-related declining sex hormones (andropause/menopause) are mediated by NO–oxygen sensing ( Berchner-Pfannschmidt et al, 2007 ; Hickok et al, 2013 ), causing a hypoxic stress condition and dysregulation of the cellular biology of amyloidosis ( Cheboub et al, 2019 ; Ahmed et al, 2022 ), which is counteracted by autophagy ( Chuang et al, 2018 ; Wang and Le, 2019 ; Wang and Zhang, 2019 ), along with the epithelial-to-mesenchymal transition (EMT) ( Byrne et al, 2016 ; Kim I. et al, 2022 ; Ribatti, 2022 ; Mohamed et al, 2023 ). A regionally restricted oxygen perfusion is a cyclic/chronic hypoxic environment that can lead to degenerative pathologies such as hypertrophy, atrophy, fibrosis, and neoplasm due to developing localized hypoxia ( Figure 1 ).…”

“…Androgen deficiency/deprivation caused drastic endothelial dysfunction, resulting in reduced blood flow (ischemia/hypovascularity) to the prostate gland ( Angrimani et al, 2020 ; Jin Cho and Pyo, 2020 ; Yoon et al, 2020 ), causing an ischemia–hypoxia stress tissue microenvironment ( Thurmond et al, 2015 ; Byrne et al, 2016 ). Hypoxia stress caused the induction of amyloidosis-autophagy-EMT cell signaling interactions, beginning with amyloidosis ( Cheboub et al, 2019 ; Phua, 2021 ) to allow cells to enter a dormant/resting stage ( Audas et al, 2016 ; Mizejewski, 2017 ; Pavliukeviciene et al, 2019 ). Age-related amyloidoses ( Rubel et al, 2020 ; Tasaki et al, 2021 ) are increasingly being discussed in the mainstream literature, including a range of organs: brain/Alzheimer’s ( Shea et al, 2019 ; Schweighauser et al, 2022 ), renal amyloidosis ( Gupta N. et al, 2020 ; Herrera, 2021 ; Gurung and Li, 2022 ), eyes/Alzheimer’s retinopathy ( Mirzaei et al, 2020 ), type 2 diabetes/Alzheimer’s ( Wang and Westermark, 2021 ), and cardiac amyloidosis ( Garcia-Pavia et al, 2021 ; Hänselmann et al, 2022 ).…”

“… 2. Nitric oxide signaling: association of endothelial dysfunction and nitric oxide signaling in the pathogenesis of Alzheimer’s disease ( Ahmed et al, 2022 ) and reduction of estrogen, which lowers nitric oxide bioavailability and induces amyloid deposition, have been observed ( Cheboub et al, 2019 ). 3.…”

The Etiology and Pathophysiology Genesis of Benign Prostatic Hyperplasia and Prostate Cancer: A New Perspective

“…Central to testosterone-vascular-inflamm-ageing triad is the early induction of amyloidosis and autophagy, which play a role in early tumor suppression in terms of the cell regulation pathways, and in their dysregulation in late stages where they act as tumor promoters [86][87][88][89][90]; this correlates to "ageing autophagy" [91][92][93][94]. Short term estrogen reduction using aromatase inhibitor in the adult Wistar male rat alters the prostatic function by reducing nitric oxide availability, inducing amyloid deposition and limiting the differentiation of basal cells through a lobe specific p63-overexpression [95]. Incidentally, these findings can be equated with amyloidosis and autophagy.…”