Wir verwenden standardmäßig essenzielle Cookies (Anmeldung, deine gespeicherten Ziele/Stacks). Mit deiner Erlaubnis aktivieren wir außerdem datenschutzfreundliche Analytik (Vercel Web Analytics, anonyme Ladezeit-Metriken) und Fehler-Replay-Diagnostik (Sentry — DOM-Snapshots nur, wenn ein Fehler auftritt), damit wir Bugs schneller beheben können. Mehr über Cookies erfahren

Los4.2

Losartan – Forschung

Überwiegend Mechanismus / Beobachtung

7 begutachtete Studien

Was die Evidenz sagt

Überwiegend Mechanismus / Beobachtung

Die meisten Studien zu Losartan sind mechanistisch oder beobachtend statt RCTs, die einen klinischen Effekt messen — betrachte die Ergebnisse als vorläufig.

Die meiste Evidenz stammt aus mittelwertigen randomisierten Studien, veröffentlicht 2001–2022 mit einer typischen Studiengröße von 1,513 Teilnehmenden.

Basierend auf 7 Studien · 3 RCTs · 11,314 Teilnehmende insgesamt

Konfidenz

Mittlere Konfidenz

Nach Outcome

Blood pressure & strokeLIFE zeigte, dass Losartan kardiovaskuläre Ereignisse — vor allem durch weniger Schlaganfälle — über Atenolol hinaus bei gleicher Blutdrucksenkung reduzierte · Monate bis Jahre
Überwiegend Mechanismus / Beobachtung4 Studien
Muscle aging & sarcopenia (animal)
Überwiegend Mechanismus / Beobachtung4 Studien
Aging & healthspan (emerging)
Zu wenige bewertete Studien2 Studien
Kidney & renal health
Zu wenige bewertete Studien1 Studie

Stetige Forschung

1 Studie in den letzten 5 Jahren

200120112022

1RCTn=9,193 · very large study2002

Losartan reduced cardiovascular morbidity and mortality — driven by a reduction in stroke — more than atenolol at equal blood-pressure lowering.

Dahlöf, Devereux, Kjeldsen, Julius, Beevers, de Faire · Lancet (London, England) (2002)

LIFE randomized trial in hypertensives with left-ventricular hypertrophy
Losartan cut the primary cardiovascular endpoint beyond atenolol at the same blood pressure
The benefit was driven by a significant reduction in fatal/non-fatal stroke

Quelle ansehen

2RCTn=1,513 · large study2001

Losartan slowed the progression of nephropathy and reduced end-stage renal disease in type 2 diabetes.

Brenner, Cooper, de Zeeuw, Keane, Mitch, Parving · The New England journal of medicine (2001)

RENAAL randomized, double-blind trial in type-2 diabetic nephropathy
Losartan reduced the composite of doubling creatinine, end-stage renal disease, or death
Renal-protective benefit largely independent of blood-pressure control

Quelle ansehen

3RCTn=608 · large study2014

Among children and young adults with Marfan's syndrome, losartan did not slow aortic-root dilation more than atenolol.

Lacro, Dietz, Sleeper, Yetman, Bradley, Colan · The New England journal of medicine (2014)

Pivotal randomized trial comparing losartan and atenolol in Marfan syndrome
No significant difference in the rate of aortic-root enlargement between groups
Counter-evidence: the compelling TGF-β rationale did not translate to a clinical win

Quelle ansehen

4Tierstudie2011

Losartan restored muscle remodeling and protected against disuse atrophy in sarcopenic mice via TGF-β blockade and IGF-1/Akt/mTOR signaling.

Burks, Andres-Mateos, Marx, Mejias, Van Erp, Simmers · Science translational medicine (2011)

In sarcopenic mice, losartan reduced fibrosis and improved muscle function after injury
It also protected aged mice from disuse atrophy during hindlimb immobilization
Acts through both TGF-β blockade and increased IGF-1/Akt/mTOR signaling

Quelle ansehen

5Tierstudie2007

Losartan (AT1-receptor blockade) normalized muscle architecture, repair, and function in fibrillin-1- and dystrophin-deficient mice by antagonizing TGF-β.

Cohn, van Erp, Habashi, Soleimani, Klein, Lisi · Nature medicine (2007)

Foundational mechanism: excess TGF-β causes failed muscle regeneration in myopathic mice
AT1 blockade with losartan normalized muscle architecture, repair, and function in vivo
Benefit shown in Marfan and Duchenne muscular dystrophy mouse models

Quelle ansehen

6Übersicht2022

The renin-angiotensin-aldosterone system is a candidate mediator of aging-associated muscle weakness, with RAS inhibition explored as a therapeutic target.

Fuloria, Subramaniyan, Meenakshi, Sekar, Chakravarthi, Kumar · Journal of biochemical and molecular toxicology (2022)

Review framing the RAAS as a driver of age-related muscle weakness / sarcopenia
Synthesizes RAS-inhibition (including ARBs) as a candidate anti-sarcopenia target
Positions the muscle-aging mechanism in the broader geroscience context

Quelle ansehen

7Tierstudie2016

Losartan promoted skeletal-muscle repair after systemic TGF-β1 elevation by blocking Smad2/3 signaling and restoring myogenic markers.

Hwang, Park, Lee, Lee, Kim, Jeong · International journal of molecular sciences (2016)

Systemically elevated TGF-β1 (from CCl4 liver injury) damaged skeletal muscle in mice
Losartan lowered p-Smad2/3 and restored Pax7, MyoD, and myogenin expression
Reinforces the TGF-β-blockade mechanism of muscle repair

Quelle ansehen

In der Forschungsbibliothek ansehen

Losartan – Forschung

Überwiegend Mechanismus / Beobachtung

Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.

Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy.

Atenolol versus losartan in children and young adults with Marfan's syndrome.

Losartan restores skeletal muscle remodeling and protects against disuse atrophy in sarcopenia.

Angiotensin II type 1 receptor blockade attenuates TGF-beta-induced failure of muscle regeneration in multiple myopathic states.

Etiopathophysiological role of the renin-angiotensin-aldosterone system in age-related muscular weakening: RAAS-independent beneficial role of ACE2 in muscle weakness.

Therapeutic Effect of Losartan, an Angiotensin II Type 1 Receptor Antagonist, on CCl4-Induced Skeletal Muscle Injury.