Studii caz-control — Cardiologie

Circulation 2026: ANXA2 crescut in inimi ischemice murine+umane; circulant ANXA2 corelat cu injuria cardiaca in IMA. KO cardiomiocitar Anxa2: mitofagie restaurata+stres oxidativ↓+inflamare↓→infarct mai mic+functie imbunatatita. Supraexprimare: mitofagie suprimata→IC agravata. Mecanism: ANXA2→blocaj

Eur Heart J 2026: Metabolismul NAD+ in BVAC. VAECs imbatranite: NAMPT↓→NAD+↓→SIRT1↓→NF-κB hiperacetilat→ICAM-1 inflammaging. Macrofage recrutate: NAMPT paradoxal↑→NAMPT extracelular→TLR4 pe VAEC→amplificare inflamatie. Deletia mieloida Nampt: FOXA2 acetilat+MMP13→distrugere colagen→calcificare accel

J Clin Invest 2026: ADAMTS7 in SMC, EC, fibroblaste (scRNA-seq ateroscleroza carotidiana umana). KO SMC sau EC specific: fara reducere ateroscleroza. Transgenic SMC-specific: ateroscleroza↑+expansiune celule spumoase SMC+capsula fibroasa↓. Transgenic EC: ateroscleroza↑. Mecanism SMC: ADAMTS7→remodel

Cardiovasc Res 2026: MCPPIR (piRNA nou) in cardiomiocite. KO MCPPIR: proliferare cardiomiocitara redusa+regenerare neonatala afectata. OE MCPPIR: proliferare crescuta+fibroza↓+functie imbunatatita post-MI. Mecanism: MCPPIR→legare HNRNPH1→previne reprimarea ARNm POC1B (via o8G)→POC1B↑→integritate cen

Cardiovasc Res 2026: Transplant alogenic iPSC-CM in primate cynomolgus. MPL+CNI+MMF: supravietuire grefa+vascularizare, fara rejectie. Fara MPL: rejectie+pierdere grefa. iPSC-CM hipo-imune: engraftment deficitar prin apoptoza (nu imun). Abatacept+tacrolimus: substitut MPL eficient, fara rejectie. Am

Int Immunopharmacol 2026: HIIT vs MICT in HFpEF murin (6 saptamani). Ambele: HTA↓+toleranta glucoza↑+toleranta efort↑+disfunctie diastolica↓+hipertrofie↓+fibroza↓. HIIT>MICT (efecte mai pronuntate). RNA-seq: necroptoza=calea pivotanta. TLR4=regulator upstream necroptoza. Antrenament→TLR4↓→RIPK1/RIPK

J Nanobiotechnol 2026: M1-macrofage produc migrasomi (M1-Migs) crescuti post-IM. M1-Migs agravează leziunea miocardica. Proteomică: GBP5 crescut in M1-Migs. KD viral GBP5: atenuare efecte M1-Migs. Mecanism: GBP5→NF-κB→apoptoza cardiomiocite. Probe clinice: migrasomi macrofagici corelati cu severitat

Nat Commun 2026: HFpEF=hiperacetilare proteine mitocondriale (predominant FAO). Dlat=transacetilaza cheie in HFpEF. OE Dlat: acetilare FAO crescuta+HFpEF agravat. KD Dlat: FAO ameliorat+HFpEF atenuat. Mecanism: Dlat acetilează HADHA la K728→HADHA inactivat→FAO inhibat→lipide intracardiace+deficit AT

Circ Res 2026: Macrofage+fibroblaste modulează FA persistenta. Modele porcine PsAF n=27+27+controale; umani PsAF n=20+controale n=7. Mapping driver→ablatie: terminare PsAF 12/14 porci. Umani: ablatie drivere→90% libertate FA la 2 ani. PsAF→fibroblaste ACTA2+PTX3 (PTX3 selectiv in regiunile driver).

Signal Transduct Target Ther 2026: cGMP-PKG suprimat in CAVD; cGMP seric invers corelat cu severitate. PKGI haploinsuficienta: calcificare agravata in vivo. PKGI silentiere→diferentiere osteogena VIC. cGMP-PKG activare (vericiguat>sildenafil>BNP): calcificare↓. Mecanism: PKGI→ULK1 fosforilat Ser556→

Circulation 2026: GRSF1 redus in cordul insuficient (pacienți DCM+modele murine). KO GRSF1 cardiac: IC spontana+hipertrofie+fibroza. OE GRSF1: atenuare IC-TAC. Mecanism: GRSF1→legare tracturi G in ARNm BCKDHB→stabilizare post-transcrip→BCKDHB↑→catabolism BCAA activ→homeostazia BCAA+mitocondrii preze

Immunity 2026: Gripa→leziuni cardiace umane+murine. Mecanism: virus gripal→infecteaza pro-DC3 circulante CCR2+→CCL2 cardiac→pro-DC3 infectate migrate la miocard→virus liberat→cardiomiocite infectate→IFN-I produs→IFNAR1 pe cardiomiocite activat→leziuni tisulare+disfunctie cardiaca. KO IFNAR1 specific

Eur Heart J 2026: n=213 obezi non-hipertensivi (MHO vs MUO), wire myograph arteriole. TCDCA (acid taurochenodeoxicolic) corelat invers cu disfunctia endoteliala. Mecanism: TCDCA→FXR→PHB1→ATF4→biosinteza serina→one-carbon metabolism→NO→protectie endoteliala. MUO=disfunctie endoteliala>MHO. Concluzie:

Eur Heart J 2026: EP4 (receptor PGE2) in HPA. Mecanism: EP4→cAMP/PKA→ANXA2 Thr208 fosforilat→β-catenin nuclear→proliferare+migrare PASMC→remodelare vasculara pulmonara. Antagonisti EP4: grapiprant+MF498→inhiba axa EP4-ANXA2-β-catenin→reduc HPA in vitro/in vivo. Concluzie: EP4/ANXA2/β-catenin=axa nou

Eur Heart J 2026: snATAC-seq+snRNA-seq pe inimi tinere vs imbatranite. ZBTB16 (factor transcriptie zinc finger-BTB) → exprimat in celule endoteliale cardiace, scazut la imbatranire. Zbtb16 KO→senescenta prematura+disfunctie diastolica+fibroza. Supraexprimare ZBTB16→reversarea imbatraniri cardiace. N