ReviewApoptosis : an international journal on programmed cell death2026
Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.
Review in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Review
- Pan-cancer analysis of the upstream regulator FDX1 in cuproptosis.Discover oncology · 2026Article
- Mitochondrial reprogramming in cervical cancer: crosstalk with tumor immunity, HPV oncogenic signaling, and therapeutic resistance.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria-associated endoplasmic reticulum membranes (MAMs) are dynamic contact points between the endoplasmic reticulum (ER) and mitochondria, governing essential cellular processes such as calcium (Ca²⁺) signaling, lipid metabolism, mitochondrial dynamics, and apoptosis. The effective movement of Ca²⁺ from the ER to mitochondria at MAMs is crucial for sustaining bioenergetics and controlling cell fate outcomes like survival or programmed cell death. Recent findings highlight the importance of MAMs in maintaining cellular balance and demonstrate their functional versatility in both healthy and diseased states. Disruption of MAM integrity and signaling is increasingly linked to the development of various diseases, including cancer. In cancer, MAMs demonstrate two regulatory roles- either promoting oncogenic functions or enhancing tumor-suppressive actions based on the molecular context and cellular environment. Changes in the structural framework of MAMs, such as variations in protein makeup and tethering distance between the ER and mitochondria, have been directly linked to several characteristics of tumor formation. Therefore, a deeper understanding of the molecular components and regulatory mechanisms governing MAM function may offer a promising avenue for the development of novel therapeutic strategies aimed at restoring proper organelle communication and counteracting cancer development and progression.
Indexed as
Identifiers
41524918What OpenQuestion 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 OpenQuestion graph.