Powstawanie męskiej niepłodności w wyniku działania receptora ACE2 -2 -> receptora białka SPIKE z koronawirusa
It is well acknowledged that the traditional RAS contains a system of finely tuned agonists and antagonists that balance blood pressure [20]. In recent years, attention has been focused on the physiological and pathophysiological studies of the human reproductive tract RAS. Classic components of the RAS have also been identified in the reproductive system, including in oocytes, granular cells, sperm cells, and Leydig cells [21,22]. Furthermore, the local RAS pathways, which are involved in reproductive events, have also been elucidated (Figure 1). ACE1, a key enzyme in the RAS, converts angiotensin I (AngI) into angiotensin II (AngII), which #!$%@? in female reproductive physiology via the AngII type 1 receptor (AT1R) and the AngII type 2 receptor (AT2R). In contrast, the functions of AngII in male reproductive events are stimulated by the AngII type 1 receptor (AT1R). ACE2, a homolog of ACE1, also emerges as a key factor in the regulation of the female and male reproductive performance that is mediated by angiotensin-(1–7) [Ang-(1–7)] [23–25]. Ang-(1–7), which is produced by ACE2, functions through the G protein-coupled receptor Mas [26,27]. To date, studies suggest that ACE3 might function in the testes of mice, rats, cows, and dogs, although ACE3 is not expressed in humans [28]. Collectively, the correct balance among the ACE1/AngII/AT1R, ACE1/AngII/AT2R and ACE2/Ang-(1–7)/Mas receptor (MasR) pathways is significant in female reproductive events, particularly follicle development, granulose-lutein (GL) cell apoptosis, ovulation, and the ACE2/Ang-(1–7)/Mas receptor axis [23,29–32]. In contrast, the ACE1/AngII/AT1R and the ACE2/Ang-(1–7)/Mas receptor pathways are involved in male fertile health, particularly steroidogenesis, epididymal contractility, and sperm cell function [21,26,33,34].
In the male reproductive tract, ACE2 is selectively expressed by adult Leydig cells in the testis. In addition, the ACE2-producing Ang-(1–7) and its receptor Mas have also been detected in the testis, and these are mainly located in the interstitial compartment and cytoplasm of the Leydig cells [26]. Reis et al. further demonstrated the strong influence of ACE2 in the male reproductive system by showing that humans with severe spermatogenesis impairment have lower levels of ACE2, Ang-(1–7), and Mas compared with fertile subjects [26]. Because the sex steroid hormone is one of the major products secreted from Leydig cells, it is suggested that ACE2 #!$%@? in the modulation of spermatogenesis. In contrast to Ace1−/− male mice, which display significantly reduced fertility, both male and female Ace2-null mice are fertile [13], which suggests that the rescue mechanisms may be regulated by other reproduction-related proteins in the testis, such as tACE1 and ACE3. Moreover, there is evidence that the testis weight is markedly reduced in Mas-deficient mice [77]. Therefore, substantial evidence implies that ACE2 regulates spermatogenesis.
LINK DO RESTREAMA-PRZECZYTAJ ZASADY Restreamowy Amber Gold: -plusujesz ten wpis -dodajesz komentarz -wysyłam pierwszym osobom link na PW -oni wysyłają otrzymane linki komentującym niżej -Ty po otrzymaniu linku robisz to samo -każdy biorący udział wygrywa #famemma
Powstawanie męskiej niepłodności w wyniku działania receptora ACE2 -2 -> receptora białka SPIKE z koronawirusa
It is well acknowledged that the traditional RAS contains a system of finely tuned agonists and antagonists that balance blood pressure [20]. In recent years, attention has been focused on the physiological and pathophysiological studies of the human reproductive tract RAS. Classic components of the RAS have also been identified in the reproductive system, including in oocytes, granular cells, sperm cells, and Leydig cells [21,22]. Furthermore, the local RAS pathways, which are involved in reproductive events, have also been elucidated (Figure 1). ACE1, a key enzyme in the RAS, converts angiotensin I (AngI) into angiotensin II (AngII), which #!$%@? in female reproductive physiology via the AngII type 1 receptor (AT1R) and the AngII type 2 receptor (AT2R). In contrast, the functions of AngII in male reproductive events are stimulated by the AngII type 1 receptor (AT1R). ACE2, a homolog of ACE1, also emerges as a key factor in the regulation of the female and male reproductive performance that is mediated by angiotensin-(1–7) [Ang-(1–7)] [23–25]. Ang-(1–7), which is produced by ACE2, functions through the G protein-coupled receptor Mas [26,27]. To date, studies suggest that ACE3 might function in the testes of mice, rats, cows, and dogs, although ACE3 is not expressed in humans [28]. Collectively, the correct balance among the ACE1/AngII/AT1R, ACE1/AngII/AT2R and ACE2/Ang-(1–7)/Mas receptor (MasR) pathways is significant in female reproductive events, particularly follicle development, granulose-lutein (GL) cell apoptosis, ovulation, and the ACE2/Ang-(1–7)/Mas receptor axis [23,29–32]. In contrast, the ACE1/AngII/AT1R and the ACE2/Ang-(1–7)/Mas receptor pathways are involved in male fertile health, particularly steroidogenesis, epididymal contractility, and sperm cell function [21,26,33,34].
In the male reproductive tract, ACE2 is selectively expressed by adult Leydig cells in the testis. In addition, the ACE2-producing Ang-(1–7) and its receptor Mas have also been detected in the testis, and these are mainly located in the interstitial compartment and cytoplasm of the Leydig cells [26]. Reis et al. further demonstrated the strong influence of ACE2 in the male reproductive system by showing that humans with severe spermatogenesis impairment have lower levels of ACE2, Ang-(1–7), and Mas compared with fertile subjects [26]. Because the sex steroid hormone is one of the major products secreted from Leydig cells, it is suggested that ACE2 #!$%@? in the modulation of spermatogenesis. In contrast to Ace1−/− male mice, which display significantly reduced fertility, both male and female Ace2-null mice are fertile [13], which suggests that the rescue mechanisms may be regulated by other reproduction-related proteins in the testis, such as tACE1 and ACE3. Moreover, there is evidence that the testis weight is markedly reduced in Mas-deficient mice [77]. Therefore, substantial evidence implies that ACE2 regulates spermatogenesis.