ReviewAging cell2021
mTORC2: The other mTOR in autophagy regulation.
Review in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 172 citations in OpenAlex.
- Rictor/mTORC2 signaling pathway protects endogenous neural stem cells to promote recovery after spinal cord injury.Neural regeneration research · 2026Article
- Review
- Inhibition of PI3K/Akt/mTOR signaling by curcumin: a novel approach to mitigate synovial fibrosis in knee osteoarthritis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Coumarins as modulators of autophagy and PI3K/mTOR signaling: implications for next-generation cancer therapies.Biomedical journal · 2026Review
- The Role of Sigmar1 in Autophagy Regulation and Disease Therapy.International journal of molecular sciences · 2026Review
- T Cell Immunosenescence in Inflammatory Skin Diseases: Pathogenesis and Therapeutic Targets.Aging cell · 2026Review
- Oleuropein modulates behavioral changes, apoptosis, autophagy, inflammation, oxidative stress-associated PI3K/Akt/mTOR pathways in TAA-Induced hepatic encephalopathy.Metabolic brain disease · 2026Article
- Nanotherapeutic Interventions for Parkinson's Disease: Modulating Pathogenic Mechanisms and Overcoming Therapeutic Obstacles.International journal of nanomedicine · 2026Review
- PI3K/AKT/mTOR axis in vascular malformations: from molecular insights to targeted clinical trials.Orphanet journal of rare diseases · 2025Review
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- From Elixirs to Geroscience: A Historical and Molecular Perspective on Anti-Aging Medicine.Molecules (Basel, Switzerland) · 2025Review
- HCMV immediate-early protein IE2 induces neurotoxicity and hearing loss by disrupting TSC2-mTOR signaling and metabolic homeostasis.Journal of neuroinflammation · 2025Article
- Asperuloside: an emerging therapeutic candidate for Parkinson's disease through molecular mechanistic insights.Inflammopharmacology · 2025Review
- Wuhu decoction regulates ROS/AMPK/mTOR pathway-mediated dendritic cells autophagy and pyroptosis for the treatment of respiratory syncytial virus-induced asthma.Journal of thoracic disease · 2025Article
- The crosstalk between autophagy and ferroptosis in pulmonary fibrosis.Journal of biomedical research · 2025Article
- PFKFB3 as a multifaceted driver and therapeutic target in castration-resistant prostate cancer.Cell death & disease · 2025Article
- Study on Autophagy Death of Alpha TC1 Clone 6 (αTC1-6) Cells Induced by Trametenolic Acid Through PI3K/AKT Pathway.Current issues in molecular biology · 2025Article
- MoSec13 combined with MoGcn5b modulates MoAtg8 acetylation and regulates autophagy inAutophagy · 2025Article
- Food insecurity impacts neuroblastoma pathogenesis in murine xenograft tumor models.Communications biology · 2025Article
- Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mechanistic target of rapamycin (mTOR) has gathered significant attention as a ubiquitously expressed multimeric kinase with key implications for cell growth, proliferation, and survival. This kinase forms the central core of two distinct complexes, mTORC1 and mTORC2, which share the ability of integrating environmental, nutritional, and hormonal cues but which regulate separate molecular pathways that result in different cellular responses. Particularly, mTORC1 has been described as a major negative regulator of endosomal biogenesis and autophagy, a catabolic process that degrades intracellular components and organelles within the lysosomes and is thought to play a key role in human health and disease. In contrast, the role of mTORC2 in the regulation of autophagy has been considerably less studied despite mounting evidence this complex may regulate autophagy in a different and perhaps complementary manner to that of mTORC1. Genetic ablation of unique subunits is currently being utilized to study the differential effects of the two mTOR complexes. RICTOR is the best-described subunit specific to mTORC2 and as such has become a useful tool for investigating the specific actions of this complex. The development of complex-specific inhibitors for mTORC2 is also an area of intense interest. Studies to date have demonstrated that mTORC1/2 complexes each signal to a variety of exclusive downstream molecules with distinct biological roles. Pinpointing the particular effects of these downstream effectors is crucial toward the development of novel therapies aimed at accurately modulating autophagy in the context of human aging and disease.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.