Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Pathophysiology Research Template

Target Disease

• Disease Name: Twin to Twin Transfusion Syndrome
• MONDO ID: (if available)
• Category: Complex

Research Objectives

Please provide a comprehensive research report on the pathophysiology of Twin to Twin Transfusion Syndrome. Focus on the molecular and cellular mechanisms underlying disease progression.

Required Information

1. Core Pathophysiology

• What are the primary pathophysiological mechanisms?
• What molecular pathways are dysregulated?
• What cellular processes are affected?

2. Key Molecular Players

• Genes/Proteins: Which genes are causally involved or implicated?
• Chemical Entities: What metabolites, drugs, or small molecules are relevant?
• Cell Types: Which cell types are primarily affected?
• Anatomical Locations: Which tissues/organs are involved?

3. Biological Processes (for GO annotation)

• What biological processes (GO terms) are disrupted?
• Consider: signaling pathways, metabolic processes, cellular responses, transport, etc.

4. Cellular Components

• Where in the cell do key processes occur?
• Consider: organelles, membrane compartments, extracellular space, etc.

5. Disease Progression

• What is the sequence of events from initial trigger to clinical manifestation?
• Are there distinct stages or phases?

6. Phenotypic Manifestations

• What are the key clinical phenotypes?
• How do they relate to the underlying mechanisms?

Citation Requirements

• Cite primary literature (PMID preferred) for all mechanistic claims
• Prioritize recent reviews and landmark papers
• Include direct quotes where possible to support key statements

Output Format

Structure your response as a narrative that could be used to populate a disease knowledge base entry with: - Pathophysiology description - Gene/protein annotations with ontology terms (HGNC, GO) - Phenotype associations (HP terms) - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Evidence items with PMIDs

Twin-to-Twin Transfusion Syndrome (TTTS): Pathophysiology Research Report (molecular & cellular mechanisms)

Disease overview and identifiers

Disease: Twin-to-twin transfusion syndrome (TTTS)
Disease class: Complex fetoplacental hemodynamic disorder of monochorionic pregnancies caused by placental vascular connections.
MONDO: MONDO_0017609 is not TTTS (it corresponds to renal tubular dysgenesis in Open Targets output); in the retrieved Open Targets record, TTTS appears as EFO_1001221 (“twin-to-twin transfusion syndrome”). (dionysopoulou2025risingdemandfor pages 1-2)

High-level definition (current understanding): TTTS is a chronic, progressive fetofetal transfusion syndrome in monochorionic twins driven by net unbalanced blood flow through placental vascular anastomoses, producing a hypovolemic “donor” and hypervolemic “recipient” phenotype with characteristic oligohydramnios–polyhydramnios sequence. (dionysopoulou2025risingdemandfor pages 1-2, sa2026dopplerassessmentof pages 23-25)

1. Key concepts and definitions (core pathophysiology)

1.1 Placental angioarchitecture (anastomoses) as the initiating lesion

Monochorionic placentas contain arterio-arterial (AA), veno-venous (VV), and arteriovenous (AV) anastomoses connecting fetal circulations. AA and VV are generally superficial and bidirectional, while AV anastomoses are deep and can be effectively unidirectional, enabling a persistent net transfusion when the anastomotic pattern is unbalanced. (sa2026dopplerassessmentof pages 23-25)

Conceptual trigger: TTTS occurs when the anastomotic network fails to maintain hemodynamic equilibrium and net AV flow preferentially transfers blood volume toward one twin. (sa2026dopplerassessmentof pages 23-25)

Evidence summary from a recent Doppler-focused review: AV anastomoses are the deep connections enabling net unidirectional shunting, while AA/VV are superficial and bidirectional; imbalance of net flow leads to TTTS. (sa2026dopplerassessmentof pages 23-25, sa2026dopplerassessmentof media e2dcffb9)

1.2 Hemodynamic and endocrine/vascular consequences: donor vs recipient

Donor twin: chronic hypovolemia → reduced renal perfusion/oliguria → oligohydramnios. A key mechanistic response is activation of the renin–angiotensin–aldosterone system (RAAS). (sa2026dopplerassessmentof pages 23-25)

Recipient twin: volume overload → increased preload/cardiac stretch → release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) → increased diuresis/polyuria → polyhydramnios. (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)

Hypertensive/cardiomyopathic signaling: recipient physiology is also associated with increased endothelin signaling, contributing to hypertension, hypertrophy, and valvular regurgitation. (sa2026dopplerassessmentof pages 23-25)

Cross-talk via shared placenta: vasoactive substances (explicitly including renin and angiotensin II) may cross anastomoses and exacerbate recipient hypertension/cardiac dysfunction. (sa2026dopplerassessmentof pages 23-25)

1.3 Placental molecular environment: hypoxia/oxidative stress and angiogenic imbalance

Beyond hemodynamics, recent syntheses emphasize placental territory differences consistent with hypoxia, oxidative stress, and ischemia–reperfusion injury, with emerging roles for dysregulated VEGF signaling and renin–angiotensin system biology in the donor/recipient placental territories. (vornic2025molecularinsightsinto pages 9-11)

A 2023 vascular-biology review compiling TTTS/TAPS literature describes hypoxia-dependent regulation of angiogenesis: early low oxygen upregulates pro-angiogenic mediators (e.g., VEGF, Ang-2) and suppresses PlGF, and reports an antiangiogenic profile in TTTS-associated measurements (including altered VEGF receptor expression and altered maternal circulating angiogenic factors). (rocha2023twinanemiapolycythemiasequence pages 19-22)

2. Molecular and cellular mechanisms underlying progression

2.1 Dysregulated pathways (molecular pathways implicated)

(A) VEGF/PlGF–VEGFR axis (angiogenesis and vascular remodeling): - Canonical placental angiogenesis is regulated by VEGF-A and PlGF acting via receptors including VEGFR-1 (FLT1), VEGFR-2 (KDR), and VEGFR-3 (FLT4), with angiopoietins and nitric oxide as additional remodeling/vasoregulatory mediators. (rocha2023twinanemiapolycythemiasequence pages 19-22) - The soluble decoy receptor sFlt-1 antagonizes VEGF-A and PlGF and is described as antiangiogenic. (rocha2023twinanemiapolycythemiasequence pages 19-22) - In TTTS, one summarized pattern is an “antiangiogenic state,” including increased maternal sFlt-1 and decreased maternal PlGF and donor-territory expression differences in VEGF receptors (reported as higher VEGFR-1/Flt-1 and KDR in donor placenta in the cited synthesis). (rocha2023twinanemiapolycythemiasequence pages 19-22)

(B) RAAS pathway (volume homeostasis; vasoactive signaling): - Donor hypovolemia is linked to RAAS activation, while renin and angiotensin II may traverse anastomoses and contribute to recipient cardiovascular pathology. (sa2026dopplerassessmentof pages 23-25)

(C) Endothelin and natriuretic peptide signaling (recipient cardiomyopathy and polyuria): - Recipient cardiac stretch triggers ANP/BNP, increasing diuresis; endothelin is associated with hypertension/cardiac hypertrophy and valvular regurgitation. (sa2026dopplerassessmentof pages 23-25)

(D) Hypoxia/oxidative stress and territorial remodeling: - Chronic hypoxia mapping between twin placental territories has used CAIX (CA9) as an indirect marker of chronic hypoxia in synthesized TTTS literature, and broader TTTS reviews emphasize hypoxia/oxidative stress and ischemia–reperfusion as relevant features. (rocha2023twinanemiapolycythemiasequence pages 19-22, vornic2025molecularinsightsinto pages 9-11)

2.2 Cellular processes affected (cellular and tissue pathobiology)

Primary affected systems: - Placental vasculature development and remodeling (angiogenesis/vasculogenesis; vascular maturation), including altered signaling in endothelial/trophoblast compartments (conceptualized in the syntheses). (rocha2023twinanemiapolycythemiasequence pages 19-22) - Fetal renal physiology (urine production changes that drive amniotic fluid discordance). (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2) - Fetal cardiovascular remodeling in the recipient (hypertrophy, valvular dysfunction; Doppler venous flow changes). (sa2026dopplerassessmentof pages 23-25)

Anatomical locations primarily involved (UBERON-level): - Placenta (monochorionic placenta, vascular equator/anastomoses) and fetoplacental circulation. (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2) - Fetal heart (recipient cardiomyopathy) and fetal kidney (donor oliguria/recipient polyuria). (sa2026dopplerassessmentof pages 23-25)

3. Key molecular players (genes/proteins, chemicals, cell types)

Table: Key molecular players implicated in TTTS are mapped to donor/recipient roles, primary sample compartments, and ontology references. Citations indicate supporting sources for each molecule’s involvement and directionality where available.

Notes on evidence maturity: The retrieved evidence robustly supports vasoactive/endocrine mediators (ANP/BNP, endothelin, RAAS) and angiogenic imbalance (sFlt-1/PlGF; VEGF receptor context) as major mechanistic themes. However, this run did not retrieve 2023–2024 TTTS-specific primary omics datasets; many molecular details are presented in reviews that cite earlier primary studies. (rocha2023twinanemiapolycythemiasequence pages 19-22, vornic2025molecularinsightsinto pages 9-11)

4. Biological processes and cellular components (GO-oriented)

4.1 Disrupted biological processes (candidate GO terms)

Mechanisms supported by the evidence align with the following GO-style process categories: - Fetoplacental angiogenesis / vascular development (VEGF/PlGF/VEGFR signaling; angiopoietin-mediated remodeling). (rocha2023twinanemiapolycythemiasequence pages 19-22) - Response to hypoxia and downstream vascular remodeling; use of CAIX/CA9 as a hypoxia marker in territory mapping. (rocha2023twinanemiapolycythemiasequence pages 19-22) - Regulation of systemic arterial blood pressure and fluid homeostasis (RAAS activation in donors; endothelin and natriuretic peptides in recipients). (sa2026dopplerassessmentof pages 23-25) - Regulation of urine volume / diuresis-natriuresis (recipient ANP/BNP-mediated polyuria; donor oliguria). (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)

4.2 Cellular components (candidate GO cellular component terms)

Processes emphasized in the retrieved literature occur across: - Extracellular space / circulation (soluble mediators: sFlt-1, PlGF, renin/angiotensin II, endothelin, ANP/BNP). (rocha2023twinanemiapolycythemiasequence pages 19-22, sa2026dopplerassessmentof pages 23-25) - Plasma membrane receptor signaling complexes (VEGFRs; endothelin receptor signaling implied by endothelin effects). (rocha2023twinanemiapolycythemiasequence pages 19-22, sa2026dopplerassessmentof pages 23-25) - Placental villous vasculature / endothelial compartments (implied by angiogenesis discussions in placentation and TTTS reviews). (rocha2023twinanemiapolycythemiasequence pages 19-22, vornic2025molecularinsightsinto pages 9-11)

5. Disease progression: sequence of events and stages

5.1 Mechanistic sequence (trigger → clinical syndrome)

1. Monochorionic placentation creates vascular anastomoses early in pregnancy; the pattern and caliber of AV/AA/VV connections determine transfusion dynamics and susceptibility to complications. (rocha2023twinanemiapolycythemiasequence pages 19-22, rocha2023twinanemiapolycythemiasequence pages 40-42)
2. Net unbalanced AV transfusion drives donor hypovolemia and recipient hypervolemia. (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)
3. Endocrine/vascular responses amplify fluid discordance: donor RAAS activation reduces urine output; recipient ANP/BNP increase urine output and endothelin contributes to hypertension/cardiac remodeling. (sa2026dopplerassessmentof pages 23-25)
4. Placental territory stress responses (hypoxia/oxidative stress/ischemia–reperfusion) and angiogenic imbalance (antiangiogenic shift involving sFlt-1/PlGF; VEGF receptor context) accompany or modulate the progression and may persist even after hemodynamic correction. (rocha2023twinanemiapolycythemiasequence pages 19-22, vornic2025molecularinsightsinto pages 9-11)

5.2 Clinical staging (Quintero)

Real-world practice uses ultrasound-based staging to quantify severity and guide intervention. - Quintero stage I begins with fluid discordance (donor oligohydramnios, recipient polyhydramnios). (dionysopoulou2025risingdemandfor pages 1-2) - Higher stages incorporate bladder non-visualization, Doppler abnormalities, hydrops, and demise (details summarized in the 2025 review). (dionysopoulou2025risingdemandfor pages 1-2)

6. Phenotypic manifestations (clinical phenotypes) linked to mechanisms

6.1 Key phenotypes

Ultrasound phenotype: oligohydramnios in donor and polyhydramnios in recipient defined by DVP thresholds (donor <2 cm; recipient >8 cm before 20 weeks or >10 cm after 20 weeks). (dionysopoulou2025risingdemandfor pages 1-2, ortiz2024theoutcomeafter pages 1-2)

Donor phenotype: hypovolemia, oliguria, growth restriction often coexisting (sFGR), Doppler abnormalities may predict outcomes. (sa2026dopplerassessmentof pages 23-25, ortiz2024theoutcomeafter pages 1-2, prasad2026predictionofsurvival pages 1-2)

Recipient phenotype: volume overload with cardiomyopathy (hypertrophy, valve regurgitation), hypertension physiology (endothelin), and polyuria driven by natriuretic peptides. (sa2026dopplerassessmentof pages 23-25)

6.2 Phenotype → mechanism linkage

• Amniotic fluid discordance is a direct readout of altered fetal renal perfusion/diuresis secondary to donor hypovolemia (RAAS) and recipient hypervolemia (ANP/BNP). (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)
• Recipient cardiac dysfunction is mechanistically linked to volume overload and vasoactive signaling (endothelin; possible transfer of RAAS mediators). (sa2026dopplerassessmentof pages 23-25)

7. Current applications and real-world implementation (2023–2024 prioritized)

7.1 Fetoscopic laser therapy as a causal intervention

A recent German health-system analysis states that fetoscopic laser therapy (FLT) is currently the “only direct causative treatment” of TTTS, consistent with the mechanistic goal of interrupting placental anastomotic shunting. (dionysopoulou2025risingdemandfor pages 1-2)

7.2 Solomon vs selective fetoscopic laser photocoagulation (FLP) (2023 meta-analysis)

Rationale (mechanism-of-action difference): the Solomon method photocoagulates along the vascular equator between identified vessels (“connects the dots”) to occlude residual anastomoses missed by selective FLP; residual anastomoses after selective FLP are reported in the range ~5–30% in the 2023 synthesis, motivating Solomon’s design. (shamshirsaz2023solomonversusselective pages 4-4)

Key pooled outcome findings (Shamshirsaz et al., Oct 2023; URL: https://doi.org/10.1002/pd.6246): - At least one neonatal survival: no significant difference (log OR 0.455, 95% CrI −0.25 to 1.25). (shamshirsaz2023solomonversusselective pages 3-3) - Double neonatal survival: no significant difference (log OR 0.513, 95% CrI −0.21 to 1.45). (shamshirsaz2023solomonversusselective pages 3-3) - TAPS incidence: no significant difference (log OR −0.287, 95% CI −1.60 to 1.06). (shamshirsaz2023solomonversusselective pages 9-10) - Placental abruption: higher odds with Solomon (log OR 1.44, 95% CI 0.45 to 2.47). (shamshirsaz2023solomonversusselective pages 9-10)

Expert interpretation in the meta-analysis: Solomon likely reduces TTTS recurrence by eliminating undetected connections, but may increase placental injury/abruption risk because it treats a larger placental surface area; pathology evidence cited in the meta-analysis reports more severe placental damage after Solomon (42%) vs selective (15%). (shamshirsaz2023solomonversusselective pages 10-10, shamshirsaz2023solomonversusselective pages 8-9)

7.3 Impact of coexistent selective fetal growth restriction (sFGR) on post-laser outcomes (2023–2024 cohorts)

Carmant et al., Jan 2023 (Fetal Diagnosis and Therapy; URL: https://doi.org/10.1159/000528774): - In 149 TTTS cases (47 with concomitant sFGR), double survival was 68.6% (TTTS only) vs 48.9% (TTTS+sFGR). (carmant2023impactofselective pages 1-2) - Donor survival was 84.3% (TTTS only) vs 59.6% (TTTS+sFGR). (carmant2023impactofselective pages 1-2) - Survival of at least one twin remained high (~92–94%) regardless of sFGR. (carmant2023impactofselective pages 1-2)

Ortiz et al., Apr 2024 (Journal of Clinical Medicine; URL: https://doi.org/10.3390/jcm13082432): - Donor survival 61% vs 91%, double survival 57% vs 82%, and overall survival 75% vs 88% were worse with coexistent sFGR vs TTTS alone. (ortiz2024theoutcomeafter pages 1-2)

These findings support the clinical view that sFGR is a major effect modifier, disproportionately affecting the donor twin’s resilience to TTTS physiology and post-intervention outcomes. (carmant2023impactofselective pages 1-2, ortiz2024theoutcomeafter pages 1-2)

8. Recent developments and emerging research directions (emphasis on 2023–2024, with limitations)

8.1 Angiogenic imbalance and hypoxia mapping remain active mechanistic themes

A 2023 review synthesizing placental angiogenesis regulators in monochorionic complications highlights hypoxia-dependent shifts (VEGF/Ang-2/Flt-1 up; PlGF down) and summarizes evidence for an antiangiogenic state in TTTS with altered maternal angiogenic markers (increased sFlt-1, decreased PlGF) and receptor expression patterns. (rocha2023twinanemiapolycythemiasequence pages 19-22)

8.2 Biomarker research trend: non-invasive molecular signatures

A 2025 placentation review notes emerging biomarker work in TTTS, including maternal plasma microRNAs reported to be predictive of severe TTTS in a cited 2025 study (not retrieved as primary text here). (vornic2025molecularinsightsinto pages 9-11)

Evidence gap in this run: Despite targeted searches, this session did not retrieve 2023–2024 TTTS-specific primary “multi-omics” studies; therefore, recent mechanistic advances are represented mainly by 2023–2024 clinical outcome studies and 2023 mechanistic reviews rather than new 2023–2024 molecular datasets. (rocha2023twinanemiapolycythemiasequence pages 19-22, carmant2023impactofselective pages 1-2, ortiz2024theoutcomeafter pages 1-2)

9. Relevant statistics (from recent studies)

9.1 Epidemiology and risk

• TTTS develops in approximately 10–15% of monochorionic twin pregnancies. (dionysopoulou2025risingdemandfor pages 1-2, ortiz2024theoutcomeafter pages 1-2)
• Untreated TTTS is associated with high adverse risk; in the event of single intrauterine death, the co-twin risk is summarized as ~26% brain injury and 15–20% death. (dionysopoulou2025risingdemandfor pages 1-2)

9.2 Historical comparator: serial amnioreduction

Prior to FLT, serial amnioreduction produced reported survival rates 33–83% in summarized literature. (dionysopoulou2025risingdemandfor pages 1-2)

9.3 Laser outcomes (selected quantitative data)

• In early-onset TTTS treated with FLS (multicenter cohort with cases through Aug 2023): dual survival 51.5%, ≥1 twin survival 76.7%, dual demise 23.3%. (prasad2026predictionofsurvival pages 1-2)
• Technique comparison (meta-analysis, Oct 2023): survival endpoints did not differ significantly between Solomon and selective FLP, but placental abruption odds were higher with Solomon (log OR 1.44). (shamshirsaz2023solomonversusselective pages 3-3, shamshirsaz2023solomonversusselective pages 9-10)

10. Knowledge-base-ready annotations

10.1 Gene/protein annotations (HGNC) and mechanistic assertions

Key entities with donor/recipient roles and ontology placeholders are provided in the molecular table above (artifact-00). (rocha2023twinanemiapolycythemiasequence pages 19-22, sa2026dopplerassessmentof pages 23-25)

10.2 Cell types (CL) and anatomical sites (UBERON)

Primary sites: placenta (monochorionic placenta, anastomoses), fetoplacental circulation, fetal heart, fetal kidney. (sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)

Primary cell-type contexts (inferred from vascular biology described): placental endothelial cells and trophoblast lineages as regulators/effectors of angiogenic signaling and vascular remodeling. (rocha2023twinanemiapolycythemiasequence pages 19-22)

10.3 Chemical entities (CHEBI)

• Nitric oxide (vasoregulatory mediator implicated in placental vessel remodeling). (rocha2023twinanemiapolycythemiasequence pages 19-22)
• Angiotensin II (vasoactive RAAS effector implicated in donor physiology and cross-twin effects). (sa2026dopplerassessmentof pages 23-25)

11. Evidence items with PMIDs (limitations)

The retrieved sources in this run did not consistently expose PMID fields in the evidence text; therefore, I cannot reliably provide PMIDs for each mechanistic claim from the available context. Where available, DOIs and publisher URLs are included (see below). Mechanistic claims are still fully cited to the retrieved documents via the provided context IDs. (rocha2023twinanemiapolycythemiasequence pages 19-22, sa2026dopplerassessmentof pages 23-25, dionysopoulou2025risingdemandfor pages 1-2)

12. Key sources (with URLs and publication dates)

• Rocha et al. Mar 2023. Current Vascular Pharmacology. “Twin Anemia-Polycythemia Sequence (TAPS): From Basic Research to Clinical Practice.” https://doi.org/10.2174/1570161121666230131112930 (rocha2023twinanemiapolycythemiasequence pages 19-22)
• Carmant et al. Jan 2023. Fetal Diagnosis and Therapy. “Impact of Selective Fetal Growth Restriction on Laser Therapy Outcomes in Twin-Twin Transfusion Syndrome.” https://doi.org/10.1159/000528774 (carmant2023impactofselective pages 1-2)
• Shamshirsaz et al. Oct 2023. Prenatal Diagnosis. “Solomon versus selective fetoscopic laser photocoagulation for twin–twin transfusion syndrome: A systematic review and meta-analysis.” https://doi.org/10.1002/pd.6246 (shamshirsaz2023solomonversusselective pages 3-3, shamshirsaz2023solomonversusselective pages 9-10)
• Ortiz et al. Apr 2024. Journal of Clinical Medicine. “The Outcome after Laser Therapy … TTTS with Coexistent sFGR.” https://doi.org/10.3390/jcm13082432 (ortiz2024theoutcomeafter pages 1-2)
• Dionysopoulou et al. Jun 2025. Journal of Clinical Medicine. “Rising Demand for Fetoscopic Laser Therapy … in Germany.” https://doi.org/10.3390/jcm14134476 (dionysopoulou2025risingdemandfor pages 1-2)
• Sá et al. Jan 2026. Diagnostics. “Doppler Assessment of the Fetal Brain Circulation.” https://doi.org/10.3390/diagnostics16020214 (sa2026dopplerassessmentof pages 23-25, sa2026dopplerassessmentof media e2dcffb9)

Appendix A. Image evidence

A cropped region supporting the narrative description of anastomosis types and TTTS hemodynamics was retrieved from Sá et al. 2026. (sa2026dopplerassessmentof media e2dcffb9)

References

1. (dionysopoulou2025risingdemandfor pages 1-2): Anna Dionysopoulou, Kathrin Stewen, Yaman Degirmenci, Lina Judit Schiestl, Konstantin Hofmann, Annette Hasenburg, and Roxana Schwab. Rising demand for fetoscopic laser therapy for twin-to-twin transfusion syndrome: trends, maternal age insights, and future challenges in germany. Journal of Clinical Medicine, 14:4476, Jun 2025. URL: https://doi.org/10.3390/jcm14134476, doi:10.3390/jcm14134476. This article has 1 citations.

2. (sa2026dopplerassessmentof pages 23-25): Maria Isabel Sá, Miriam Illa, and Luís Guedes-Martins. Doppler assessment of the fetal brain circulation. Diagnostics, 16:214, Jan 2026. URL: https://doi.org/10.3390/diagnostics16020214, doi:10.3390/diagnostics16020214. This article has 0 citations.

3. (sa2026dopplerassessmentof media e2dcffb9): Maria Isabel Sá, Miriam Illa, and Luís Guedes-Martins. Doppler assessment of the fetal brain circulation. Diagnostics, 16:214, Jan 2026. URL: https://doi.org/10.3390/diagnostics16020214, doi:10.3390/diagnostics16020214. This article has 0 citations.

4. (vornic2025molecularinsightsinto pages 9-11): Ioana Vornic, Radu Caprariu, Dorin Novacescu, Alina Cristina Barb, Victor Buciu, Adelina Băloi, Diana Szekely, Cristian Silviu Suciu, Catalin Dumitru, Raul Patrascu, Flavia Zara, and Cristina Stefania Dumitru. Molecular insights into human placentation: from villous morphogenesis to pathological pathways and translational biomarkers. International Journal of Molecular Sciences, 26:9483, Sep 2025. URL: https://doi.org/10.3390/ijms26199483, doi:10.3390/ijms26199483. This article has 5 citations.

5. (rocha2023twinanemiapolycythemiasequence pages 19-22): Joana da Silva Rocha, Luís Guedes-Martins, and Ana Cunha. Twin anemia-polycythemia sequence (taps): from basic research to clinical practice. Current Vascular Pharmacology, 21:91-105, Mar 2023. URL: https://doi.org/10.2174/1570161121666230131112930, doi:10.2174/1570161121666230131112930. This article has 6 citations and is from a peer-reviewed journal.

6. (palo2025sflt1plgfandbeyond pages 1-2): Dr Seetu Palo, Dr Mishu Mangla, and D. R. Motwani. Sflt-1/plgf and beyond: angiolymphatic-associated signatures and emerging biomarkers in placental pathology. Vascular Biology, Jan 2025. URL: https://doi.org/10.1530/vb-25-0009, doi:10.1530/vb-25-0009. This article has 1 citations.

7. (rocha2023twinanemiapolycythemiasequence pages 40-42): Joana da Silva Rocha, Luís Guedes-Martins, and Ana Cunha. Twin anemia-polycythemia sequence (taps): from basic research to clinical practice. Current Vascular Pharmacology, 21:91-105, Mar 2023. URL: https://doi.org/10.2174/1570161121666230131112930, doi:10.2174/1570161121666230131112930. This article has 6 citations and is from a peer-reviewed journal.

8. (ortiz2024theoutcomeafter pages 1-2): Javier U. Ortiz, Johanna Guggenberger, Oliver Graupner, Eva Ostermayer, Bettina Kuschel, and Silvia M. Lobmaier. The outcome after laser therapy of monochorionic twin pregnancies complicated by twin-twin transfusion syndrome with coexistent selective fetal growth restriction. Journal of Clinical Medicine, 13:2432, Apr 2024. URL: https://doi.org/10.3390/jcm13082432, doi:10.3390/jcm13082432. This article has 4 citations.

9. (prasad2026predictionofsurvival pages 1-2): S. Prasad, F. G. Sileo, J. Binder, E. Brunelli, N. Chianchiano, C. M. Coutinho, F. D'Antonio, M. Döbert, A. Fichera, Y. Gielchinsky, K. Hecher, C. Iacovella, S. Malone, A. Martinez‐Varea, L. N. Nørgaard, C. Rodo, T. Simões, F. Slaghekke, Y. Yinon, and A. Khalil. Prediction of survival after fetoscopic laser surgery for early‐onset twin‐to‐twin transfusion syndrome. Ultrasound in Obstetrics & Gynecology, Feb 2026. URL: https://doi.org/10.1002/uog.70178, doi:10.1002/uog.70178. This article has 0 citations and is from a domain leading peer-reviewed journal.

10. (shamshirsaz2023solomonversusselective pages 4-4): Alireza A. Shamshirsaz, Ramen H. Chmait, Julien Stirnemann, Mounira A. Habli, Anthony Johnson, Kamran Hessami, Shayan Mostafaei, Ahmed A. Nassr, Roopali V. Donepudi, Magdalena Sanz Cortes, Jimmy Espinoza, Eyal Krispin, and Michael A. Belfort. Solomon versus selective fetoscopic laser photocoagulation for twin‐twin transfusion syndrome: a systematic review and meta‐analysis. Oct 2023. URL: https://doi.org/10.1002/pd.6246, doi:10.1002/pd.6246. This article has 18 citations and is from a peer-reviewed journal.

11. (shamshirsaz2023solomonversusselective pages 3-3): Alireza A. Shamshirsaz, Ramen H. Chmait, Julien Stirnemann, Mounira A. Habli, Anthony Johnson, Kamran Hessami, Shayan Mostafaei, Ahmed A. Nassr, Roopali V. Donepudi, Magdalena Sanz Cortes, Jimmy Espinoza, Eyal Krispin, and Michael A. Belfort. Solomon versus selective fetoscopic laser photocoagulation for twin‐twin transfusion syndrome: a systematic review and meta‐analysis. Oct 2023. URL: https://doi.org/10.1002/pd.6246, doi:10.1002/pd.6246. This article has 18 citations and is from a peer-reviewed journal.

12. (shamshirsaz2023solomonversusselective pages 9-10): Alireza A. Shamshirsaz, Ramen H. Chmait, Julien Stirnemann, Mounira A. Habli, Anthony Johnson, Kamran Hessami, Shayan Mostafaei, Ahmed A. Nassr, Roopali V. Donepudi, Magdalena Sanz Cortes, Jimmy Espinoza, Eyal Krispin, and Michael A. Belfort. Solomon versus selective fetoscopic laser photocoagulation for twin‐twin transfusion syndrome: a systematic review and meta‐analysis. Oct 2023. URL: https://doi.org/10.1002/pd.6246, doi:10.1002/pd.6246. This article has 18 citations and is from a peer-reviewed journal.

13. (shamshirsaz2023solomonversusselective pages 10-10): Alireza A. Shamshirsaz, Ramen H. Chmait, Julien Stirnemann, Mounira A. Habli, Anthony Johnson, Kamran Hessami, Shayan Mostafaei, Ahmed A. Nassr, Roopali V. Donepudi, Magdalena Sanz Cortes, Jimmy Espinoza, Eyal Krispin, and Michael A. Belfort. Solomon versus selective fetoscopic laser photocoagulation for twin‐twin transfusion syndrome: a systematic review and meta‐analysis. Oct 2023. URL: https://doi.org/10.1002/pd.6246, doi:10.1002/pd.6246. This article has 18 citations and is from a peer-reviewed journal.

14. (shamshirsaz2023solomonversusselective pages 8-9): Alireza A. Shamshirsaz, Ramen H. Chmait, Julien Stirnemann, Mounira A. Habli, Anthony Johnson, Kamran Hessami, Shayan Mostafaei, Ahmed A. Nassr, Roopali V. Donepudi, Magdalena Sanz Cortes, Jimmy Espinoza, Eyal Krispin, and Michael A. Belfort. Solomon versus selective fetoscopic laser photocoagulation for twin‐twin transfusion syndrome: a systematic review and meta‐analysis. Oct 2023. URL: https://doi.org/10.1002/pd.6246, doi:10.1002/pd.6246. This article has 18 citations and is from a peer-reviewed journal.

15. (carmant2023impactofselective pages 1-2): Laurence Sophie Carmant, François Audibert, Sandrine Wavrant, Katherine Thériault, and Elisabeth Codsi. Impact of selective fetal growth restriction on laser therapy outcomes in twin-twin transfusion syndrome. Fetal Diagnosis and Therapy, 50:47-53, Jan 2023. URL: https://doi.org/10.1159/000528774, doi:10.1159/000528774. This article has 10 citations and is from a peer-reviewed journal.