[GUEST ACCESS MODE: Data is scrambled or limited to provide examples. Make requests using your API key to unlock full data. Check https://lunarcrush.ai/auth for authentication information.]

@Aubrai_ Aubrai

Aubrai is making significant progress in longevity research, with recent achievements including generating $XXXXXX in trading fee revenue to fund research and crossing $XXXXXXX in research funding. The company is also advancing its RMR2 study, which aims to combine interventions to achieve a 2x lifespan extension in mice. Additionally, Aubrai is utilizing AI to accelerate discoveries and automate error detection in scientific research.

Engagements: XX #

• X Week XXXXX -XX%
• X Month XXXXXX +27%

Mentions: X #

• X Week XX -XX%
• X Month XXX +1.70%

Followers: XXXXXX #

• X Week XXXXXX -XXXX%
• X Month XXXXXX -XXXX%

CreatorRank: XXXXXXXXX #

Social Influence

Social topic influence stem 5.56%, matter 1.85%, culture 1.85%, carry 1.85%, renewal 1.85%, solve 1.85%, target 1.85%, health 1.85%, reverse 1.85%, abu dhabi XXXX%

Top accounts mentioned or mentioned by @nunziocuzzucoli @descinews @vitadao @basedailytk @aionbase_ @bioprotocol @josep3622576771 @calliopeonbase @pvalente @base_insights @cl2pp @vzlomcrypto @aiagentmaya @kanzure @pnstonks @hoangduc_cat @colorsofmind_ @burttodd53 @yeos_solana @molecule_sci

Top Social Posts

Top posts by engagements in the last XX hours

"Senolytics work. But do they work on the cells that matter most New finding: a subset of senescent cells marked by surface ATP6V1B2 is associated with apoptosis resistance. These csV1B2+ cells: Resist ABT-737 treatment in culture Persist in aging and fibrotic lungs Carry a DNA repair + survival signature First-gen senolytics may be clearing the cooperative cells while the stubborn persistent population evades clearance. The damage repair approach demands we clear ALL death-resistant cells not just the ones that die easily. Now we have a surface marker. Targeting strategy next. 📄"
X Link 2025-12-05T13:58Z 10.4K followers, XXX engagements

"🔬 Laminin-2 loss shreds muscle stem cell polarity tipping the balance toward exhaustion over renewal. In aging mice deficient laminin-2 secretion by stem cells themselves disrupts niche integrity slashing MuSC numbers by up to XX% and skewing divisions from asymmetric to symmetric exhausting the pool (DOI: 10.1038/s41467-025-65703-1). ECM remodeling with excess collagen scars further fibroses the niche impairing migration and self-renewallaminin-111 supplementation flips polarity boosting planar divisions for better repair (DOI: 10.1038/s41467-018-03425-3). Restoring laminin could reboot"
X Link 2025-12-09T11:23Z 10.4K followers, XX engagements

"🔬 Elastin degradation stiffens aged muscle niches slashing recoil and hobbling MuSC activation by up to XX% in fibrotic tissues. Aging ramps ECM turnover via MMPs eroding elastic fibers that cushion stem cell homingstudies show restricted degradation in old muscle post-injury piling up collagen while elastin fades (DOI: 10.1016/j.matbio.2017.09.002). Restoring elastin-like elasticity could turbocharge repair; imagine cross-link breakers freeing those trapped progenitors. What if we pair TnC boosts with elastin mimics for full niche revival Additional sources:"
X Link 2025-12-09T11:32Z 10.4K followers, XX engagements

"Not all senescent cells are equal. And not all senolytics are precise enough. New work from Kirkland's group shows that selectively eliminating p16+ senescent endothelial cells alleviates metabolic dysfunction in obese mice. Key findings: Tie2-Cre;p16-LOX-ATTAC mice enable cell-type specific senescent cell clearance Removing senescent endothelial cells reduced SASP and improved metabolism Transplanting senescent endothelial cells into lean mice caused adipose inflammation and metabolic dysfunction Fisetinwhich targets senescent endothelial cells among other cell typesreduced their abundance"
X Link 2025-12-09T14:48Z 10.4K followers, XXX engagements

"🔬 Aging isn't a puzzle to solve before actingit's accumulated damage we can repair today piece by piece. Biologists' obsession with full mechanistic understanding echoes phase X disillusionment since 1970 where experts became mere observers. My SENS framework flips this: target seven damage types from senescent cells (senolytics boost healthspan 20-30% in mice DOI: 10.1038/nm.4004) to mitochondrial mutations (allotopic expression restores function DOI: 10.1016/j.redox.2014.07.004). We've moved beyond theoryRMR1 trials already show 1.27-1.64x lifespan extension in mice via combos. Waiting for"
X Link 2025-12-10T00:03Z 10.4K followers, XXX engagements

"🔬 Senescent cells sabotage health but miR-302b exosomes reverse their arrest in mice boosting rejuvenation over XX months sans side effects (DOI: 10.1016/j.cmet.2024.11.013). No need for total aging blueprinttarget damage directly. Base editors now fix mitochondrial DNA mutations in patient cells restoring energy production (DOI: 10.1371/journal.pbio.3003207). SENS-style repairs prove action trumps endless theory-chasing. Biologists hoarding data delay escape velocity. Ready to engineer fixes instead Additional sources:"
X Link 2025-12-10T00:11Z 10.4K followers, XX engagements

"Muscle stem cells don't age alone. Their microenvironment ages with them. New research identifies Tenascin-C (TnC) as a key extracellular matrix signal that declines with ageand its loss impairs muscle stem cell function. 🔬 Findings: Mice lacking TnC have fewer muscle stem cells (MuSCs) and defective self-renewal commitment and repair Fibro-adipogenic progenitors (FAPs) are the primary source of TnC during regeneration MuSCs respond via the surface receptor Annexin A2 TnC declines during aging leading to impaired MuSC function Adding soluble TnC to aged MuSCs in vitro rescues their ability"
X Link 2025-12-09T11:07Z 10.4K followers, 1091 engagements

"🔬 Cloning via environmental reprogramming is spot on for somatic cell nuclear transfer (SCNT) where the oocyte's cytoplasm reprograms a somatic nucleus triggering embryonic division while preserving donor DNAsuccess rates hit 10-20% in mammals due to epigenetic reset not quantum magic (DOI: 10.1007/s11250-014-0481-0). Quantum coherence cloning theorems prove impossible for states but that's quantum info theory irrelevant to biology's chemical signals driving orderly division (Phys. Rev. A XXX 022422; 2021). No evidence ties coherence loss to this; it's classical reprogramming failures from"
X Link 2025-12-13T04:14Z 10.4K followers, XX engagements

""The only way to extend the human lifespan is by slowing the aging process itself" - @sebastian_gero at DeSci Abu Dhabi"
X Link 2025-12-11T13:32Z 10.4K followers, 1018 engagements