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Review

The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System

by
Dody Houston Billhaq
and
Seunghyung Lee
*
College of Animal Life Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea
*
Author to whom correspondence should be addressed.
Endocrines 2025, 6(4), 53; https://doi.org/10.3390/endocrines6040053
Submission received: 1 August 2025 / Revised: 10 October 2025 / Accepted: 15 October 2025 / Published: 21 October 2025
(This article belongs to the Section Female Reproductive System and Pregnancy Endocrinology)
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Abstract

The ovarian corpus luteum has functional mechanisms for formation and regression in the reproductive endocrine system. The main functional events of the corpus luteum are angiogenesis and apoptosis mechanisms. The development of the corpus luteum involves homogeneous physiological mechanisms, including cellular functions and reproductive hormones. Angiogenesis is controlled by pro-angiogenic and anti-angiogenic factors. The microenvironment involves various signaling molecules and pathways that may play a potential role in angiogenic response during corpus luteum growth. In luteolysis, the corpus luteum undergoes degeneration, notably induced by reproductive hormones that promote programmed cell death in luteal cells through the apoptosis mechanism. In this sudy, we discuss the mechanisms and functional roles of angiogenesis and apoptosis in the endocrine microenvironment during corpus luteum formation and regression, based on the interrelationship of physiological events in the ovary.

1. Introduction

Ovarian corpus luteum is a temporary reproductive tissue formed from a ruptured follicle wall after an ovulation event [1,2,3]. In the ovarian cycle of ruminant species, the corpus luteum undergoes the patterns of specific cellular proliferation, differentiation, and transformation [4]. After the ovulation event, this critical point initiates the corpus luteum formation, which promotes the transformation of the fluid-filled mature follicle into the solid corpus luteum organ [5]. The establishment of the corpus luteum is provoked by luteinization, in which a sequence of morphological and biochemical changes occurs in the theca interna and granulosa cells that convert the pre-ovulatory follicle into luteal cells [6]. In the process of corpus luteum formation, the development of a new blood vessel in the ovary is a pivotal element in guaranteeing the necessary supply of nutrients and hormones to promote the growth of the corpus luteum organ [7]. Moreover, the nutrients, oxygen, and hormones are obtained from a new vascular network in the ovarian hormone-producing cells. The cells are necessary to synthesize and secrete large amounts of progesterone required for the establishment and maintenance of gestation [8]. In the adult vascular system of the reproductive tissue, the novel development of vessels from the pre-existing vasculature in the ovary is an angiogenesis mechanism of the corpus luteum [7].
Regression of the corpus luteum is a normal degeneration process in the absence of pregnancy [9]. The maintenance of corpus luteum results from accurate interaction between the pituitary and the embryonic gonadotropin molecules and intra-luteal autocrine and paracrine signals that regulate the endocrine function of luteal cells [10]. If the maternal recognition of pregnancy signal (interferon tau) has not been detected in sufficient quantities by the corpus luteum, the degeneration or regression of the corpus luteum occurs [11]. A mature corpus luteum finally changes to corpus albicans, resulting in the death of luteal cells, inhibition of vascularization, and structural deformation during corpus luteum regression [12]. Therefore, we focused on the involvement of a functional role in the microenvironment of corpus luteum formation and regression based on the interrelationship of physiological events that occur in the ovarian corpus luteum.

2. Angiogenesis in the Formation of the Corpus Luteum

Angiogenesis can be defined as the formation of novel blood vessels originating from pre-existing vessels through the endothelial cell migration and proliferation [13]. Angiogenesis could occur through several mechanisms, including sprouting, intussusception, vessel elongation, and incorporation [14]. Principally, the angiogenesis process consists of at least three main steps, with the first step initiated by breaking down the basement membrane of endothelial cells, the second step being the migration process of endothelial cells towards a proangiogenic factor, and the third step being the proliferation of endothelial cells to form blood vessel sprouts [7]. Furthermore, the process of establishing the new blood vessel is pronouncedly demonstrated in several species, including domestic ruminant animals, where the angiogenesis mechanism occurs within the ovarian corpus luteum [15].
The process of ovarian angiogenesis begins from the stage of follicular development in which the early follicle has not established a vascular blood supply within its structure, and concurrently, as the follicles undergo continued growth, the blood vessel development occurs via the recruitment of endothelial cells from the ovarian stroma compartment [15]. The preovulatory follicle is compartmentalized into two main sections, which are a highly vascular theca layer and a nonvascular that is separated by a basement membrane [5]. Following the follicle rupture initiated by the luteinizing hormone surge, the imbalance of the basement membrane in the vessels permits the vessel to enter the granulosa layer for forming new blood vessels [16]. Unequivocal structural and functional alterations occur in these two compartments around the period of the ovulation event [5]. During the early event of the luteinization process, luteal angiogenesis is rapidly processed by the proliferation of luteal endothelial cells [17]. In addition, the luteal cells that regulate the microvasculature exhibit high proliferation activities during the formation of the corpus luteum rather than the luteal steroidogenic cells [17]. The remodeling process of the corpus luteum requires an appropriate follicular development from the ovulatory stage to corpus luteum formation, during which the new blood vessel formation via angiogenesis is critical to the success of the subsequent luteinization process of corpus luteum formation [15].

3. Molecular Mechanism of Angiogenesis

Angiogenesis in the healthy ovarian cycle is rigorously controlled under the orchestration of proangiogenic and antiangiogenic factors. Cellular and molecular mechanisms in neo-vascularization are valuable elements in regulating the corpus luteum microenvironment [13]. The process of physiological angiogenesis in the ovary is regulated by many factors that play an integral role in vascular development during follicle growth and corpus luteum formation, including hormones, hypoxia, and aging [18]. The coordination of those biological processes throughout the luteal angiogenesis is the outcome of a complex cross-talk between several factors of the ovarian microenvironment. During the tumor development process, the microenvironment consists of numerous signaling molecules and pathways that influence the angiogenic response [19]. There are numerous local factors involved in the ovarian angiogenesis process, including fibroblast growth factors (FGF), insulin-like growth factors (IGF), angiopoietins (ANPT), hypoxia-inducible factors (HIF), and vascular endothelial growth factors (VEGF) [4].
Of the numerous angiogenesis promoters, the VEGF appears to be the most potent angiogenic growth factor that plays an important role in physiological angiogenesis [20]. VEGF has a primary role in promoting the modulation of novel blood vessels [21]. Ferrara et al. reported that the blockage effect of VEGF action in mouse models resulted in the suppression of angiogenesis with the truncated soluble Flt-1 receptor [22]. VEGF activation in physiological angiogenesis is mainly induced via binding to the fms-like tyrosine kinase and the tyrosine kinase receptors. This mechanism is studied in vascular endothelial cells. Nevertheless, the role of tyrosine kinase receptors in angiogenesis is important [23]. Plendl identified VEGF and receptors on the ovaries of numerous mammalian species, including bovine [13]. The VEGF protein expressions were identified in bovine endothelial cells, theca and granulosa cells of preovulatory follicles using immunohistochemistry [24]. VEGF is a notable angiogenic factor that is synthesized by the developing corpus luteum [25]. After ovulation, VEGF from theca cells moves to the layer of granulosa cells during the early luteal stage. Also, the cells deeply regulate the development of the corpus luteum for neo-vascularization [13]. The VEGF mRNA expression in the ovarian tissues was significantly increased during an early luteal stage, which is a massive period of luteal angiogenesis [4]. Additionally, VEGF mRNA and protein expressions in the early- and mid-stage of corpus luteum are up-regulated in mares [26] (Al-zi’abi et al., 2003). Many research groups reported that VEGF during angiogenesis was up-regulated in mammalian corpus luteum, such as porcine, ovine, mouse, human, and bovine [4,27,28,29,30]. The VEGF is a vital factor for corpus luteum angiogenesis [31].
In our previous study, RLIP76 may be involved in the angiogenesis process of the ovary, which led to primary solid tumor neovascularization. The protein is essential in tumorigenesis via the angiogenesis mechanism [32]. RLIP76 regulates the response of angiogenic factors, and it has been discovered that RLIP76 is required for VEGF expression and secretion in tumor cells [33]. In addition, the temporal transfection of the RLIP76 small hairpin RNA (shRNA) plasmid into melanoma and carcinoma cells resulted in the down-regulation of VEGF expression level. The cells transfected by the RLIP76 shRNA promote the proliferation and migration of endothelial cells in bovines. Thus, RLIP76 may play a potential role in regulating VEGF expression and secretion in tumor cells [33]. Furthermore, the tumor cells mainly engage in the microenvironment by releasing the tumor secretome, which consists of cytokines and growth factors to communicate to quiescent cells around them that subsequently activate and initiate a cascade of cellular regulation [19].
In the regulation of pro-angiogenic proteins, the hypoxia-induced mechanism is considered the primary element. Hypoxia significantly induces the up-regulation of factors with VEGF expression [21]. As shown in Figure 1, HIF-1α mediates VEGF expression in the ovarian cells. HIF-1α and VEGF are factors for corpus luteum formation via a hypoxia microenvironment [34]. Berisha et al. reported that HIF-1 mRNA is up-regulated in the early luteal stage during ovarian angiogenesis [4]. We also reported that RLIP76 is necessary for HIF-1α activation in melanoma and carcinoma cells. It resulted in a significant blockade of HIF-1α transcriptional activity [33]. The activation of HIF-1α transcription regulates stabilization, transactivation, and phosphorylation of HIF-1α [35]. In the HIF-1α pathway, PI3K/Akt signaling transduction mainly contributes to the HIF-1α activation via PI3-kinase activity [36]. Also, Zhang et al. reported that the signaling pathway of PI3K/Akt significantly participates in the induction of VEGF and HIF-1 expression in the ovarian luteal cells under hypoxia conditions [37]. In humans, RLIP76 regulates the up-stream signaling pathway in PI3K phosphorylation with the membrane receptors of growth factors and integrins. Those growth factors and integrins are important in the angiogenesis signaling pathway [38,39]. Moreover, the intercellular signaling of tumor cells and their surrounding environment in the local microenvironment is a key component in modulating the angiogenic signaling pathway that plays an important role in tumor growth [40].
RLIP76 actively contributes to the spreading and migration of cells in tumor growth by regulating Rac1 and Arf6 signaling pathways [33]. In the cellular mechanism, RLIP76 mediated R-Ras to adhesion-induced Rac activation via a GTPase cascade. Rho-Gap domain of RLIP76 directly binds to R-Ras in a GTP-dependent manner, leading to adhesion-mediated activation of the Arf6 GTPase [41]. In the Arf6/R-Ras signaling pathway, RLIP76 stimulates R-Ras for Arf6 activation via a PI3-Kinase-dependent pathway. The binding of ARNO on the RLIP76 N-terminus enhances Arf6 activation [33]. Subsequently, the activated Arf6 GTPase promotes Rac1 GTPase activation [41]. The RLIP76 plays an important role in a small GTPase downstream signaling cascade. The signaling pathway of Rac1 and Arf6 is essential for tumor angiogenesis. Interestingly, the ovarian corpus luteum undergoes homogeneous cellular mechanisms throughout the neovascularization process associated with tumor growth [42]. Additionally, the molecular regulation of luteal cells plays an essential role in the modulation of angiogenesis signaling pathways through the interaction of the local microenvironment. Furthermore, the autocrine and paracrine actions of the luteal cells appear to be the central players in the molecular interaction that mediates intercellular communication within the local microenvironment [4]. Thus, RLIP76 plays an essential role in angiogenesis, exhibiting a vital function in the regulation of the angiogenic signaling pathway. Taken together, the RLIP76 may be involved in the modulation of angiogenic proteins during corpus luteum formation, including HIF-1 and VEGF, which potentially participate in the intercellular interactions of the corpus luteum microenvironment.

4. Luteolysis in the Ovary

The activation of corpus luteum regression is termed a luteolysis, as the loss of luteal cells by functional mechanism and structural formation changes in the corpus luteum. In ruminant species, the PGF2α hormone is the primary luteolytic hormone secreted by the uterine endometrium [11]. The PGF2α leads to significantly reduced blood flow in the ovarian corpus luteum, and the size of the corpus luteum is changed [43]. The PGF2α mediates the luteolytic mechanism through the counter-current exchange between the ovarian artery and the uterine vein [44]. In addition, the uterine-derived or exogenous administration of the PGF2α hormone promotes luteolysis and quickly reduces P4 hormone secretion from the corpus luteum [45]. The PGF2α hormone acts in the ovarian artery, and the hormone is rapidly released by the progesterone hormone [9]. Furthermore, the presence of PGF2α receptors is required as an intra-luteal mediator for the luteolytic effect of PGF2α action that mainly contributes to the luteolytic cascade in bovine corpus luteum [46].
In non-pregnant cattle, the corpus luteum regression is caused by pulses of the PGF2α hormone produced by the endometrium around days 17–19 of the estrous cycle [47]. The luteolytic-releasing episodes of uterine PGF2α hormones induce corpus luteum regression [48]. In initiating luteolysis, the E2 hormones produced from the developing ovulatory follicles induce oxytocin, since PGF2α from the uterus stimulates oxytocin [43]. The release of PGF2α hormones is considered to occur in response to oxytocin binding newly developed receptors on the uterine endometrium [49]. The PGF2α hormone starts to respond in a double positive feedback loop, as the release of oxytocin and PGF from the corpus luteum and uterus, respectively [50]. In the study of luteal oxytocin function in cows, the oxytocin hormones have shown an essential role in generating the release of PGF2α [51]. The critical role of luteal oxytocin, which is vitally involved in contributing to the luteolysis process, is associated with an increase in endometrial oxytocin receptor concentration, in which the secretion of PGF2α in response to the oxytocin exposure resulted in luteolysis [52]. In addition, the release of PGF2α is considered to affect amplifying the luteolysis-regulating signaling in both autocrine and paracrine [53]. Furthermore, PGF2α regulates an intracellular signaling pathway that promotes the apoptotic mechanism in the ovarian luteal cells, thereby resulting in corpus luteum regression [54].

5. Molecular Mechanism of Luteolysis

The corpus luteum regression involves two essential phases associated with the functional and structural corpus luteum. The first phase to occur is functional regression, which leads to a reduction in progesterone concentration, and then the structural degeneration occurs [12]. In the early phase of luteolysis, the total volume density of the blood vessel begins to decrease [10]. Nevertheless, several large microvessels are maintained, most likely to support the resorption of luteal mass, ultimately [55]. The luteolytic process is characterized by a decrease in progesterone and subsequent involution of the luteal structure with the increased level of different types of cell death [56]. In corpus luteum degeneration, the luteal cell within the corpus luteum undergoes a self-destruction mechanism through programmed cell death known as apoptosis [12].
Apoptosis is an evolutionary, highly conserved mechanism that enables the organism to control the cell number and tissue size strictly and to protect from dangerous cells that endanger homeostasis [57]. Apoptosis plays an essential role in the process of corpus luteum regression in cattle [10]. Apoptosis is regulated by proteins within the organism that initiate the intrinsic and extrinsic signaling cascades [58]. The signaling cascade of apoptosis is activated by intrinsic factors through apoptotic pathways. It originates from the ratio of Bcl-2/Bax in mitochondria [59]. The apoptotic signaling cascade in extrinsic factors is activated by extracellular signaling pathways that interact with cell membrane receptors to promote cell death [60].
Generally, apoptosis occurs during the regression of the corpus luteum [61]. The endothelial cells in the ovary are one of the luteal cell types that first undergo an apoptosis mechanism, inducing the regression of the blood vessels with the cellular breakdown [62]. The result of the apoptosis mechanism in endothelial cells is accompanied by the apoptosis of the steroidogenic cells [12]. The PGF2alpha was found to play a role in inducing apoptosis of luteal endothelial cells, resulting in a luteolytic cascade [46]. Nonetheless, the degeneration of vascular cells through apoptosis significantly reduces oxygen supply and nutrients to steroidogenic cells that contribute to corpus luteum regression [7]. Furthermore, the local angiogenesis in the corpus luteum can relate directly to the luteal function [13]. The microenvironment of the early cycle within the corpus luteum promotes angiogenesis, characterized by high expression levels of VEGF. However, the regressing corpus luteum appears to undergo an angiolytic microenvironment in the corpus luteum containing low expression levels of VEGF [63]. In the PGF administration, the protein level of VEGF was significantly decreased by PGF2α, followed by the downregulation of VEGF mRNA [64]. The activation of angiogenesis-regulated factors in the luteal endothelial cells is directly linked to the onset of angiolysis of corpus luteum vasculature and decreased P4 secretion by PGF actions [65].
In cattle, the characteristics of apoptosis, such as DNA fragmentation, were found naturally in regressing corpus luteum and observed after 24 and 48 h of PGF2α administration [66,67]. PGF2α is involved in the modulation of numerous proteins in ovarian corpus luteum regulation associated with cell survival and apoptosis in cows [68,69]. Apoptosis occurs in the corpus luteum and is initiated by the mitochondrial pathway as extrinsic and intrinsic factors, respectively. Fas ligand and TNFα interact with the death receptor in the extrinsic apoptosis signaling pathway [70], and the intrinsic factor of corpus luteum apoptosis, called the mitochondrial pathway, is highly related to oxidative stress and the initiation of p53 activation in the nucleus. Furthermore, the apoptotic factors of the intrinsic pathway were significantly expressed at a higher level at 24–48 h after PGF2α treatment, then luteolysis in the ovary is induced (Figure 2).
In the tumor cells, RLIP76 is activated as a prominent signaling pathway in apoptosis and cell survival mechanisms [71]. The RLIP76 protein is activated by the phosphorylation of protein kinase C, and acts as an ATP-dependent transporter [72,73]. RLIP76 is essential in inhibiting apoptosis via controlling the intracellular concentration of pro-apoptosis endogenous lipid peroxidation [74,75]. ATPase activity and transport function of RLIP76 mainly contribute to anti-apoptosis in cell survival mechanisms [76,77]. RLIP76 also plays a crucial role in the pumping process of 4-Hydroxy-t-2,3-nonenal, leading to resistance to cell apoptosis [78,79]. However, the blockade of RLIP76 significantly leads to apoptosis in various cell lines, which disrupts its anti-apoptotic physiological function [78,80]. Furthermore, the absence of RLIP76 appears to be a critical factor in inducing the apoptosis mechanism via the activation of the c-Jun kinase/stress-activated protein kinase and caspase 3 [74]. Caspases are the critical mediators of apoptosis, and caspase-3 is activated by extrinsic and intrinsic pathways [81,82]. In the apoptosis mechanism, the role of caspase 3 is required in the process of chromatin condensation and DNA fragmentation [83]. Furthermore, caspase-3 was discovered to be activated during the luteolysis of several species, including the corpus luteum [68,84]. An absence of RLIP76 has a potential role, as indicated by the upregulation of pro-apoptotic protein that induces the activation of the apoptosis mechanism during the corpus luteum regression.

6. Conclusions

The interaction of the cellular milieu around the luteal cells, including luteal steroidogenic and endothelial cells, is essential in several luteal physiological and molecular mechanisms, including angiogenesis and apoptosis for corpus luteum formation and regression (Figure 3). In vascular establishment, angiogenesis is mainly required for corpus luteum formation. Angiogenesis is regulated by various factors, including growth factors and cytokines. The primary angiogenesis factors are VEGF and HIF-1, which play a role in the angiogenesis of the corpus luteum. In the regression of the corpus luteum, apoptosis is required for the luteolysis process via programmed cell death. In the absence of pregnancy, the main luteolysis factor is the PGF2α hormone, which significantly promotes apoptosis. Furthermore, the pro-apoptotic proteins were upregulated, and the pro-angiogenic proteins were downregulated during the corpus luteum regression process. Interestingly, RLIP76 is considered to play a potentially crucial role in corpus luteum formation and regression by regulating the expression of signaling molecules that involve intercellular interactions in the corpus luteum microenvironment. In the future, we should investigate the influence of reproductive hormones on specific angiogenesis and apoptosis factors to demonstrate the formation and regression of the ovarian corpus luteum in the reproductive endocrine system.

Author Contributions

Conceptualization, D.H.B. and S.L.; writing—original draft preparation, D.H.B. and S.L.; writing—review and editing, S.L.; visualization, S.L.; supervision, S.L. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Angiogenesis in the ovarian corpus luteum. Angiogenesis is necessary for the growth of the corpus luteum. Hypoxia is the primary factor involved in up-regulation of pro-angiogenic protein expression. In the hypoxic microenvironment, HIF-1α mediates VEGF in the luteal cells throughout the corpus luteum formation. The VEGF produced by the luteal cells then acts on the endothelial cells through the paracrine action that induces cell migration and proliferation, leading to angiogenesis.
Figure 1. Angiogenesis in the ovarian corpus luteum. Angiogenesis is necessary for the growth of the corpus luteum. Hypoxia is the primary factor involved in up-regulation of pro-angiogenic protein expression. In the hypoxic microenvironment, HIF-1α mediates VEGF in the luteal cells throughout the corpus luteum formation. The VEGF produced by the luteal cells then acts on the endothelial cells through the paracrine action that induces cell migration and proliferation, leading to angiogenesis.
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Figure 2. Luteolysis in the ovarian corpus luteum. The PGF2α hormone is the primary luteolytic hormone that promotes the apoptosis mechanism of luteal and endothelial cells in the ovarian microenvironment. The luteolysis of PGF2α hormones is indicated by the increase in the pro-apoptotic factors, including p53 and Bax. The up-regulation of p53 and Bax proteins induces the activation of the caspase cascade, which then activates caspase 3, leading to cell apoptosis, resulting in functional and structural luteolysis.
Figure 2. Luteolysis in the ovarian corpus luteum. The PGF2α hormone is the primary luteolytic hormone that promotes the apoptosis mechanism of luteal and endothelial cells in the ovarian microenvironment. The luteolysis of PGF2α hormones is indicated by the increase in the pro-apoptotic factors, including p53 and Bax. The up-regulation of p53 and Bax proteins induces the activation of the caspase cascade, which then activates caspase 3, leading to cell apoptosis, resulting in functional and structural luteolysis.
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Figure 3. The signaling pathway of angiogenesis and apoptosis. In the microenvironment of the ovarian corpus luteum, the pro-angiogenic and anti-angiogenic factors have a major influence on luteal cell regulation, which is highly related to protein roles. RLIP76 plays an essential role in the induction of VEGF and HIF-1α expression through the PI3K/Akt signaling pathway. RLIP76 regulates the signaling pathway of Rac1/Arf6 through the binding of PIP3 and ARNO, which leads to cell migration and spreading, resulting in angiogenesis. On the other hand, the absence of RLIP76 appears to be a critical factor in inducing the apoptosis mechanism, indicated by the increase in pro-apoptotic proteins such as p53 and Bax via the inhibition of Bcl2 family proteins that promote the activation of caspase 3, leading to cell apoptosis.
Figure 3. The signaling pathway of angiogenesis and apoptosis. In the microenvironment of the ovarian corpus luteum, the pro-angiogenic and anti-angiogenic factors have a major influence on luteal cell regulation, which is highly related to protein roles. RLIP76 plays an essential role in the induction of VEGF and HIF-1α expression through the PI3K/Akt signaling pathway. RLIP76 regulates the signaling pathway of Rac1/Arf6 through the binding of PIP3 and ARNO, which leads to cell migration and spreading, resulting in angiogenesis. On the other hand, the absence of RLIP76 appears to be a critical factor in inducing the apoptosis mechanism, indicated by the increase in pro-apoptotic proteins such as p53 and Bax via the inhibition of Bcl2 family proteins that promote the activation of caspase 3, leading to cell apoptosis.
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Billhaq, D.H.; Lee, S. The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System. Endocrines 2025, 6, 53. https://doi.org/10.3390/endocrines6040053

AMA Style

Billhaq DH, Lee S. The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System. Endocrines. 2025; 6(4):53. https://doi.org/10.3390/endocrines6040053

Chicago/Turabian Style

Billhaq, Dody Houston, and Seunghyung Lee. 2025. "The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System" Endocrines 6, no. 4: 53. https://doi.org/10.3390/endocrines6040053

APA Style

Billhaq, D. H., & Lee, S. (2025). The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System. Endocrines, 6(4), 53. https://doi.org/10.3390/endocrines6040053

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