Evidence map›Paper›PMID 34744606›Full record

ReviewFrontiers in neuroscience2021

Cal'MAM'ity at the Endoplasmic Reticulum-Mitochondrial Interface: A Potential Therapeutic Target for Neurodegeneration and Human Immunodeficiency Virus-Associated Neurocognitive Disorders.

Jessica Proulx, In-Woo Park, Kathleen Borgmann

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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  9. [Icariside Ⅱ Inhibits Hepatitis B Virus and Modulates Mitochondrial FissionSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jessica ProulxDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center (HSC), Fort Worth, TX, United States.
In-Woo ParkDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center (HSC), Fort Worth, TX, United States.
Kathleen BorgmannDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center (HSC), Fort Worth, TX, United States.
University of North Texas · US

Funding

Astrocyte-TAAR1 & METH in HANDR01DA039789 · NIDA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI MATHIS, J. MICHAEL · 2015 to 2019
$1.7M
The ER-mitochondria interface in astrocytes during METH exposure and HIV-1 infectionF31DA053151 · NIDA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI PROULX, JESSICA MICHELLE · 2021 to 2022
$58k
NIDA NIH HHS F31 DA053151NIDA NIH HHS R01 DA039789
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is a multifunctional organelle and serves as the primary site for intracellular calcium storage, lipid biogenesis, protein synthesis, and quality control. Mitochondria are responsible for producing the majority of cellular energy required for cell survival and function and are integral for many metabolic and signaling processes. Mitochondria-associated ER membranes (MAMs) are direct contact sites between the ER and mitochondria that serve as platforms to coordinate fundamental cellular processes such as mitochondrial dynamics and bioenergetics, calcium and lipid homeostasis, autophagy, apoptosis, inflammation, and intracellular stress responses. Given the importance of MAM-mediated mechanisms in regulating cellular fate and function, MAMs are now known as key molecular and cellular hubs underlying disease pathology. Notably, neurons are uniquely susceptible to mitochondrial dysfunction and intracellular stress, which highlights the importance of MAMs as potential targets to manipulate MAM-associated mechanisms. However, whether altered MAM communication and connectivity are causative agents or compensatory mechanisms in disease development and progression remains elusive. Regardless, exploration is warranted to determine if MAMs are therapeutically targetable to combat neurodegeneration. Here, we review key MAM interactions and proteins both

Indexed as

astrocytescalcium dysregulationER stressmitochondria-associated ER membranesmitochondrial dysfunctionneuropathologyUnfolded protein response

Identifiers

PMID34744606
PMCPMC8566765
OpenAlexW3208260357

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.