Hair-Cell Regeneration

Demonstrated components today: In living mice, scientists have converted the cochlea’s own supporting cells into new, functioning hair cells — not by adding foreign cells, but by switching on the genetic program the ear used to build them in the first place. Single-cell sequencing confirms the converted cells turn on hundreds of true hair-cell genes, and in noise-deafened animals this has produced measurable, partial recovery of hearing.

The capability being built toward: a one-time treatment that reawakens a deaf person’s own supporting cells to regrow native hair cells in place. When fully built, this would restore hearing using the patient’s living tissue — no device and no foreign cells. Today it is robust in mice and early in larger animals; the direction is clear and the human translation is the work that remains.

The cochlea’s hair cells sit amid supporting cells that, during development, were held back from becoming hair cells by Notch signaling and pushed toward their fate by the master gene Atoh1 and the Wnt pathway. Crucially, a subset of supporting cells — those expressing Lgr5, the same stem-cell marker found in the gut — retain latent competence to become hair cells. Albert Edge’s group at Mass Eye and Ear and Harvard showed that blocking Notch with a gamma-secretase inhibitor (LY411575) raises Atoh1 and drives Lgr5+ supporting cells to differentiate into new hair cells, with partial hearing recovery after acoustic trauma. Forcing Atoh1 directly, or combining it with the transcription factor Ikzf2, pushes conversion further: Zhiyong Liu’s team at the Chinese Academy of Sciences generated prestin-expressing outer-hair-cell-like cells in adult mice — a long-standing barrier, since prestin is the motor protein that makes outer hair cells amplify sound. The frontier challenge is doing this efficiently in the mature human cochlea, where the regenerative program is most deeply silenced, and producing properly patterned, fully mature inner and outer hair cells rather than partial conversions.

Notch inhibition regrows hair cells after noise damage. Albert Edge’s team at Mass Eye and Ear and Harvard Medical School delivered the Notch-blocking drug LY411575 into noise-deafened mouse ears; nearby Lgr5-expressing supporting cells transdifferentiated into new hair cells, yielding a measurable partial recovery of hearing (Neuron, 2013).

Lgr5 marks the cells with regenerative competence. Edge and colleagues identified Lgr5+ cells — carrying the same stem-cell marker as intestinal stem cells — as the specific supporting-cell population that becomes new hair cells under Notch inhibition, pinpointing the ear’s resident progenitor pool.

Atoh1 plus Ikzf2 makes true outer-hair-cell-like cells. Zhiyong Liu’s group at the Institute of Neuroscience, Chinese Academy of Sciences, co-induced Atoh1 and Ikzf2 in adult mouse supporting cells and produced prestin-positive outer-hair-cell-like cells — overcoming the long-standing failure to make cells expressing the key amplifier protein (eLife, 2021).

Sequencing confirms a deep fate switch. In the same work, single-cell RNA sequencing showed the converted cells upregulated 729 hair-cell genes and downregulated 331 supporting-cell genes, a far more advanced conversion than earlier attempts achieved.

The program is conserved from regenerating species. Birds and fish naturally regrow hair cells lifelong from supporting cells using these same Atoh1/Notch/Wnt signals; mammalian work aims to reactivate the version mammals silenced after birth.

Combination signaling pushes conversion further. Adding Wnt activation and co-factors such as TUB and ZNF532 has been shown to boost Atoh1-mediated regeneration in mouse cochleae, mapping the cocktail needed for efficient human conversion.

Research & institutions: Albert Edge (Mass Eye and Ear / Harvard Medical School); Zhiyong Liu (Institute of Neuroscience, Chinese Academy of Sciences); Stefan Heller (Stanford University); Neil Segil (USC / Caltech); Andy Groves (Baylor College of Medicine); Jeffrey Karp (Brigham and Women’s Hospital / MIT); Frequency Therapeutics; the NIH National Institute on Deafness and Other Communication Disorders (NIDCD); Decibel Therapeutics; University of Michigan Kresge Hearing Research Institute.

Demonstrated components today: Children born profoundly deaf from a single faulty gene have had usable hearing restored by a one-time dose delivering a working copy of that gene to the cochlea’s own cells. In published human trials, most treated children gained speech perception and could hear and converse; some have now been followed for years with hearing that holds. This is the field’s first true cure-by-restoration, repairing the native cells rather than bypassing them.

The capability being built toward: gene therapy that corrects the broad range of single-gene deafness faults — OTOF, GJB2, and dozens more — ideally restoring the patient’s own hair cells to full native function. When fully built, a child identified at newborn screening could be treated once and hear normally for life. Today this is real and clinical for OTOF-related deafness; extending it to the many other deafness genes, and to adults, is the direction still being built.

Many inherited deafnesses trace to one broken gene. In DFNB9, the OTOF gene fails to make otoferlin, a protein inner hair cells need to release neurotransmitter onto the auditory nerve — the hair cells are structurally present but cannot signal. Because the cells survive, supplying a working OTOF gene can switch them back on. The preferred route is exactly this: restore the cochlea’s own native cells. An adeno-associated virus (AAV) carrying a functional gene copy reaches the inner ear; the cells take it up and resume normal function. OTOF is an ideal first target because the protein acts inside the cell that receives the gene and the hair cells are intact. The same logic extends to GJB2 (connexin-26), the most common cause of inherited deafness, where the protein recycles potassium to keep the cochlea’s electrical gradient — though GJB2 is harder, because connexin-26 is needed in several cell types and developmental windows, and a gene large or split-delivery problem applies to some other targets. The work ahead is covering more genes, treating before or just after birth when the cochlea is most rescuable, and confirming durability across the human lifespan.

One delivery restored hearing in children born deaf. A team co-led by Zheng-Yi Chen (Mass Eye and Ear / Harvard Medical School) with Yilai Shu at Fudan University’s Eye & ENT Hospital delivered an AAV carrying a working OTOF gene to children with DFNB9; five of six gained hearing over 26 weeks, with four robust responses and recovered speech perception (The Lancet, January 2024).

It works in both ears, with speech and conversation. A follow-on bilateral trial restored hearing and speech in children treated in both ears, enabling them to localize sound and hold conversations (Nature Medicine, 2024).

The benefit is durable. Mass General Brigham and Harvard reported that restored hearing from OTOF gene therapy has lasted years in treated children, with continued gains in speech (2026 trial update).

OTOF was chosen because it repairs the native cell. In DFNB9 the inner hair cells survive but cannot signal without otoferlin, so restoring the gene reactivates the patient’s own cells — the preferred native route rather than replacement.

Connexin-26 is the next major target. Multiple groups have used AAV to restore GJB2/connexin-26 expression and rescue hearing in conditional knockout mice, addressing the most common inherited deafness, with combination approaches (e.g. added dexamethasone) improving the rescue (Advanced Science / Molecular Therapy, 2025).

Delivery has been validated up to primates. Cochlear AAV gene transfer with optimized vectors and noninvasive routes has achieved efficient, safe transduction of inner hair cells in nonhuman primates, a key step toward broad human use (Nature Communications, 2022).

Research & institutions: Zheng-Yi Chen (Mass Eye and Ear / Harvard Medical School); Yilai Shu (Fudan University Eye & ENT Hospital); Eliot Shearer and Margaret Kenna (Boston Children’s Hospital); Lawrence Lustig (Columbia University); Hinrich Staecker (University of Kansas); Regeneron; Eli Lilly / Akouos; Decibel Therapeutics; Sensorion; the NIH NIDCD; Karen Avraham (Tel Aviv University).

Demonstrated components today: A hair cell is useless if it is not wired to the auditory nerve. Researchers have shown in animals that a single growth factor delivered to the inner ear can regrow the lost connections — the ribbon synapses — between hair cells and nerve fibers, recovering hearing function even when the hair cells themselves were intact. This directly targets “hidden hearing loss,” the synaptic damage that standard hearing tests miss.

The capability being built toward: a therapy that rebuilds the hair-cell-to-nerve wiring — both to treat hidden hearing loss on its own and to ensure that regrown or gene-corrected hair cells actually connect and transmit sound. When fully built, this becomes the essential companion step that turns a regenerated hair cell into restored hearing. Today the animal evidence is strong and consistent; human delivery and dosing are the emerging work.

Each inner hair cell connects to the auditory nerve through specialized ribbon synapses. Noise and aging can destroy these synapses while leaving the hair cell and the nerve-cell body alive — a silent injury called cochlear synaptopathy or hidden hearing loss, where the audiogram looks normal but speech-in-noise falls apart. The signaling molecule that builds and maintains these synapses is neurotrophin-3 (NT-3), normally supplied by supporting cells. Gabriel Corfas and colleagues at the University of Michigan showed that boosting NT-3 in the cochlea increases ribbon-synapse density and regenerates lost synapses after acoustic trauma, recovering function. Because the spiral-ganglion nerve cells survive for months to years after the synapse is lost, there is a long therapeutic window to reconnect them. Delivery has been demonstrated both by placing NT-3 on the round-window membrane and by AAV-driven overexpression. The emerging challenge is translating dose, timing, and delivery to humans, and pairing synapse regeneration with hair-cell regeneration so newly made cells are functionally wired in.

Round-window NT-3 regenerates lost synapses. Researchers showed that delivering neurotrophin-3 onto the round-window membrane of noise-exposed animals regenerated cochlear ribbon synapses after acoustic overexposure, restoring connections between hair cells and nerve (Scientific Reports, 2016).

NT-3 controls synapse density and recovery. Gabriel Corfas’s group at the University of Michigan demonstrated that NT-3 regulates ribbon-synapse density in the cochlea and induces synapse regeneration after acoustic trauma, with hearing recovery (eLife, 2014).

Gene-delivered NT-3 protects the wiring. AAV-mediated NT-3 overexpression was shown to protect cochleae against noise-induced synaptopathy, demonstrating a one-time gene-therapy route to the same effect (Gene Therapy, 2018).

The target is hidden hearing loss. This work addresses the large class of patients who lose synaptic connections — not hair cells — to noise or age, whose hearing tests look normal but who struggle to follow speech in noise.

The repair window is long. Because spiral-ganglion neuron cell bodies and central projections survive for months to years after synapse loss, there is an extended window in which reconnection can restore hearing.

Antibody agonists can mimic the effect. Trk-receptor agonist antibodies acting like BDNF and NT-3 promoted neuron survival, neurite extension, and synapse restoration in cochlear models relevant to hidden hearing loss, widening the therapeutic toolkit (PLOS One, 2019).

Research & institutions: Gabriel Corfas (University of Michigan Kresge Hearing Research Institute); M. Charles Liberman (Mass Eye and Ear / Harvard Medical School); Sharon Kujawa (Mass Eye and Ear); Tejbeer Kaur (Creighton University); Lisa Goodrich (Harvard Medical School); the NIH NIDCD; Decibel Therapeutics; Pipeline Therapeutics; Stanford University; Albert Edge (Mass Eye and Ear).

Demonstrated components today: When a person’s hair cells and supporting cells are entirely gone — so there is nothing left to reawaken in place — scientists can grow new hair cells from the body’s own stem cells. From a patient’s own reprogrammed (iPS) cells, labs have generated functioning, mechanosensitive hair-cell-like cells and even self-organizing inner-ear organoids that produce hair cells wired to nerve cells. This is a backup route for the most severe loss, secondary to regrowing cells from the ear’s own supporting cells.

The capability being built toward: a way to manufacture patient-matched replacement hair cells (or otic progenitors) and regenerate them from the cochlea’s own supporting cells where the native ones are gone, so they engraft, mature, and connect. When fully built, this would extend restoration to the hardest cases that in-place regeneration cannot reach. Today this is a frontier lab capability — cells are made and characterized, but reliable in-place regeneration within a living human cochlea remains unsolved.

Where degeneration has destroyed both hair cells and the Lgr5+ supporting cells needed to regrow them, there is no resident population left to convert — so cells must be supplied. Stefan Heller’s group at Stanford pioneered stepwise protocols that guide embryonic and induced pluripotent stem (iPS) cells through an ectoderm and otic-progenitor stage to mechanosensitive hair-cell-like cells bearing stereocilia bundles. Building on this, three-dimensional culture produced inner-ear organoids: from a single stem-cell aggregate, tuning the TGF, BMP, FGF, and Wnt pathways generates otic vesicles that mature over about two months into sensory epithelia with hair cells that are electrophysiologically similar to native ones and are contacted by neurons. In the laboratory, because these organoids can be derived from a patient’s own cells, the resulting tissue is immune-matched — demonstrated so far in cultured lab models, not in animals or humans. Generating patient-specific replacement inner-ear tissue for clinical use remains a capability being built toward, not a present clinical treatment. This route is focused on noninvasive, endogenous regeneration as the preferred Healthy direction: current organoid work guides how to regenerate cells in place within the fluid-filled cochlea, position correctly, and wire in — an invasive delivery challenge that in-place reprogramming sidesteps. Under the Healthy standard, the preferred direction remains noninvasive, endogenous, harm-free restoration whenever possible; endogenous regeneration is the preferred route reserved for cases where the ear’s own supporting cells cannot do the job.

Functional hair cells made from iPS cells. Stefan Heller’s team at Stanford generated mechanosensitive hair-cell-like cells — complete with stereociliary bundles — from both embryonic and induced pluripotent stem cells, the first functional inner-ear sensory cells created in the lab (Cell, 2010).

Self-organizing inner-ear organoids. Koehler, Hashino, and colleagues at Indiana University generated inner-ear organoids from human pluripotent stem cells containing functional hair cells whose electrophysiology matched native sensory cells, innervated by bipolar neurons forming synapses (Nature Biotechnology, 2017).

This is the backup for total loss. The approach is reserved for cases where hair cells and the Lgr5+ supporting cells are both gone, leaving nothing in place to reawaken — making in-place regeneration the preferred route, with cell replacement treated as a research route for cases of total loss.

Lab-grown cells are immune-matched to the patient. Because the starting iPS cells come from the patient, the resulting hair cells are genetically self in culture — a laboratory result that avoids the rejection problem of donor tissue.

Organoid maturation parallels the real ear. Functional development of the mechanosensitive hair cells in these organoids was shown to parallel native vestibular hair cells, confirming the lab-grown cells follow authentic developmental steps (Nature Communications, 2016).

Research & institutions: Stefan Heller (Stanford University); Eri Hashino and Karl Koehler (Indiana University / Boston Children’s Hospital); Jeffrey Holt (Boston Children’s Hospital / Harvard); Albert Edge (Mass Eye and Ear); Marcelo Rivolta (University of Sheffield); Azel Zine (University of Montpellier); the NIH NIDCD; the California Institute for Regenerative Medicine (CIRM); Rinri Therapeutics.

Demonstrated components today: Making a hair cell is not enough — it must mature into the right kind of hair cell, in the right place, with the right molecular biology. Researchers have already coaxed regenerated and stem-cell-derived cells to take on key mature features: outer-hair-cell identity with prestin (the protein that amplifies sound), inner-hair-cell identity via specific master genes, and electrical responses resembling native cells. This step turns a generic new cell into a working part of the hearing organ.

The capability being built toward: reliable control over hair-cell maturation — specifying inner versus outer fate, positioning cells along the cochlea’s pitch map, and equipping them with full mechanotransduction and amplification so they faithfully encode sound. When fully built, regenerated cells would be indistinguishable in function from the ones a person was born with. Today partial maturation, including prestin and inner-cell identity, has been achieved; complete, tonotopically tuned maturation in the adult cochlea is the emerging frontier.

The cochlea is exquisitely organized: inner hair cells transmit sound to the nerve, outer hair cells mechanically amplify it using the motor protein prestin, and both are arranged along a tonotopic map from high to low frequency. Early regeneration attempts produced immature or wrongly specified cells — often lacking prestin, so they could not amplify. Progress has been rapid. Zhiyong Liu’s group used Atoh1 with Ikzf2 to push supporting cells to genuine prestin-positive outer-hair-cell-like identity, and showed that the transcription factor Tbx2 governs inner-hair-cell fate and transdifferentiation. Stem-cell and organoid systems produce hair cells with native-like electrophysiology, demonstrating that maturation biology can be engaged in the dish. The emerging challenge is doing all of this in the adult human cochlea at once: directing each new cell to the correct inner/outer fate for its position, building functional mechanotransduction and ribbon synapses, and matching the cell’s tuning to its location on the frequency map — so the regenerated organ does not just contain hair cells but hears with fidelity.

Prestin — the amplifier protein — achieved. Zhiyong Liu’s team (Chinese Academy of Sciences) drove adult supporting cells to become prestin-positive outer-hair-cell-like cells with Atoh1 plus Ikzf2, clearing the central barrier that earlier regenerated cells lacked the amplifier protein (eLife, 2021).

Inner-hair-cell fate has its own master switch. The same group showed that the transcription factor Tbx2 is required for inner-hair-cell development and for transdifferentiation toward inner-hair-cell identity, giving a tool to specify the correct cell type (National Science Review, 2022).

Regenerated cells gain native-like electrophysiology. Stem-cell-derived and organoid hair cells display electrophysiological properties similar to native sensory hair cells, evidence that functional maturation can be induced (Nature Biotechnology, 2017).

Sequencing tracks how complete maturation is. Single-cell RNA sequencing of converted cells (729 hair-cell genes up, 331 supporting-cell genes down) provides a quantitative readout of how far a new cell has matured toward true hair-cell identity (eLife, 2021).

Maturation in organoids parallels real development. The functional development of mechanosensitive hair cells in stem-cell organoids was shown to parallel native vestibular hair cells, confirming authentic maturation steps (Nature Communications, 2016).

Co-factors refine the outcome. Genes such as TUB and ZNF532 were found to enhance Atoh1-mediated regeneration, part of mapping the full set of signals needed to mature cells correctly (2021).

Research & institutions: Zhiyong Liu (Institute of Neuroscience, Chinese Academy of Sciences); Stefan Heller (Stanford University); Eri Hashino and Karl Koehler (Indiana University / Boston Children’s Hospital); Jian Zuo (Creighton University); Andy Groves (Baylor College of Medicine); Neil Segil (USC / Caltech); Albert Edge (Mass Eye and Ear); the NIH NIDCD; University of Michigan Kresge Hearing Research Institute.

Demonstrated components today: Every therapy above is only as good as our ability to get it into the cochlea — a tiny, fluid-filled, bone-encased spiral where the hearing cells live, and where clumsy access can itself destroy hearing. Researchers have developed atraumatic routes — delivery through the round-window membrane and controlled cochlear delivery — and engineered AAV vectors that, in animals up to primates, transduce nearly all the target hair cells without damaging cochlear function. The first human cochlear gene-therapy deliverys have already been done safely in the OTOF trials.

The capability being built toward: a standardized, safe delivery platform — the right noninvasive route paired with vectors and formulations that reach the correct cells, at the correct dose, across the whole length of the cochlea, in adults as well as children, without harming residual hearing or spreading beyond the ear. When fully built, this is the shared infrastructure every regeneration and gene therapy rides on. Today delivery is proven in animals and demonstrated in first human use; refining it for routine, full-cochlea, adult human therapy is the open frontier.

The cochlea is a fluid-filled labyrinth sealed in dense temporal bone, with the round-window membrane and the oval window as the main natural entry points. Therapies are introduced either by permeating across the round-window membrane through needle-free carriers, ideally without disturbing the inner-ear fluids that hearing depends on. The molecular cargo — a gene, a reprogramming factor — is usually carried by adeno-associated virus. Vector engineering has advanced quickly: synthetic and ancestral serotypes such as Anc80L65 and engineered AAV variants achieve high transduction of inner and outer hair cells after round-window delivery in mice, and optimized vector-plus-noninvasive-route combinations have transduced inner hair cells efficiently and safely in nonhuman primates. Key constraints remain: AAV’s limited packaging size for large genes, age- and cell-type-dependent transduction, achieving uniform coverage from cochlear base to apex, and confining the therapy to the treated ear. The frontier work is converting these animal and first-in-human successes into a reliable, atraumatic, full-cochlea delivery standard for adult patients.

First human cochlear gene therapy was delivered safely. The OTOF trials delivered AAV gene therapy into children’s inner ears and restored hearing without unacceptable harm, proving that controlled human cochlear delivery is feasible (The Lancet, 2024).

Ancestral AAV transduces the whole sensory epithelium. Round-window delivery of Anc80L65 achieved highly efficient transduction of both inner and outer hair cells in mice — a major improvement over conventional vectors (PNAS / Mol Ther, 2017).

Complete inner-hair-cell transduction without dysfunction. Cochlear gene therapy with ancestral AAV in adult mice achieved complete transduction of inner hair cells while preserving cochlear function, showing the adult ear can be reached safely (2017).

Validated in primates with the right route. Choice of vector combined with the right noninvasive approach enabled efficient cochlear gene transfer in nonhuman primates, a critical bridge to humans (Nature Communications, 2022).

Engineered variants reach supporting cells too. Screened AAV variants were shown to permit efficient transduction access to both supporting cells and hair cells — important because supporting cells are the source for in-place regeneration (Cell Discovery, 2019).

Transduction depends on cell type and age. Studies mapping AAV tropism found outer hair cells most accessible in early life and inner hair cells at the mature stage, defining the dosing and timing rules delivery must respect (Scientific Reports, 2025).

Research & institutions: Luk Vandenberghe (Mass Eye and Ear / Harvard Medical School, Anc80L65); Zheng-Yi Chen (Mass Eye and Ear / Harvard); Gwenaelle Geleoc and Jeffrey Holt (Boston Children’s Hospital); Hinrich Staecker (University of Kansas); Lawrence Lustig (Columbia University); Akouos / Eli Lilly; Decibel Therapeutics; Sensorion; the NIH NIDCD; Fudan University Eye & ENT Hospital.

Demonstrated components (today): In mice, gene therapy that re-supplies prestin (SLC26A5) to outer hair cells, and reprogramming that converts adult supporting cells into prestin-positive outer-hair-cell-like cells, have each been shown in animal models; human stem-cell organoids can grow cells bearing the prestin marker (lab model and animal).

The capability being built toward: Rebuilding a working cochlear amplifier in a damaged human ear — outer hair cells that are correctly placed, innervated, and electromotile enough to restore the ~40–60 dB of active gain and sharp frequency tuning — has not been achieved and remains a goal being built toward.

Outer hair cells are the cochlea’s active amplifier: each one changes length thousands of times per second in step with sound, pumping mechanical energy back into the basilar membrane. That motion is powered by prestin (the SLC26A5 protein), a voltage-driven motor packed into the cell’s wall that shortens and lengthens the cell as its membrane voltage swings, using intracellular chloride ions as its voltage sensor. This electromotility supplies roughly 40–60 dB of gain and sharpens frequency tuning, which is why the faintest sounds become audible and why neighboring pitches can be told apart. Restoring it means rebuilding not just any hair cell but the specific prestin-driven motility that makes mammalian hearing sensitive and selective.

Prestin is the motor protein of outer hair cells. Jing Zheng, David Z. He, Peter Dallos and colleagues at Northwestern University identified prestin (SLC26A5) in 2000 (Nature), showing that expressing it in non-motile kidney cells conferred the voltage-dependent length changes and nonlinear capacitance that power cochlear amplification.

Prestin’s voltage sensor is the chloride ion. Dominik Oliver, Bernd Fakler and co-workers (then Universität Tübingen, with Peter Dallos) reported in Science (2001) that intracellular anions — chloride and bicarbonate — act as the voltage sensor for prestin, and that removing them abolishes the fast electromotility thought to drive the amplifier.

Disabling prestin’s motor collapses the cochlear amplifier. Mary Ann Cheatham, Peter Dallos and colleagues at Northwestern, using prestin-knockout mice and a knockin (“499”, V499G/Y501H) mouse that places prestin in the membrane but cripples its motility, showed in The Journal of Physiology and in Neuron (2008) that outer-hair-cell electromotility falls by over 90% and sound sensitivity drops roughly 100-fold (about 40–60 dB), with loss of sharp frequency tuning.

A single master gene, Ikzf2/Helios, switches on the outer-hair-cell program. Karen Steel and colleagues (Wellcome Sanger Institute and King’s College London) reported in Nature (2018) that the “cello” mutation in Ikzf2 (Helios) causes early hearing loss and loss of prestin-dependent electromotility, and that forcing Ikzf2 into inner hair cells pushes them toward an outer-hair-cell identity and confers electromotility.

Adult supporting cells can be reprogrammed into prestin-positive outer-hair-cell-like cells. Zhiyong Liu and colleagues at the Institute of Neuroscience, Chinese Academy of Sciences (Shanghai) reported in eLife (2021) that simultaneous expression of Atoh1 and Ikzf2 converts adult cochlear supporting cells into prestin-expressing outer-hair-cell-like cells in vivo — the first such conversion in adult animals.

Gene therapy that re-supplies prestin can restore hearing in prestin-deficient mice. Cochlear delivery of Slc26a5 — including a 2025 Neuron study using a B8 enhancer to drive native-like prestin expression, and an AAV-ie-K558R–prestin approach (Signal Transduction and Targeted Therapy, 2022) — restored outer-hair-cell prestin and recovered auditory thresholds, partially or substantially, in Slc26a5-knockout mice.

Research & institutions: Northwestern University (Jing Zheng, Peter Dallos, Mary Ann Cheatham, David Z. He), Creighton University (David Z. He), UCL Ear Institute (Jonathan Ashmore), Universität Tübingen and University of Marburg (Dominik Oliver), University of Freiburg (Bernd Fakler), Wellcome Sanger Institute and King’s College London (Karen Steel), Institute of Neuroscience, Chinese Academy of Sciences (Zhiyong Liu), University of Chicago (Eduardo Perozo, prestin cryo-EM), Harvard Medical School / Mass Eye and Ear (M. Charles Liberman), Stanford University (Stefan Heller, inner-ear organoids), and Boston Children’s Hospital / Harvard (Jeffrey Holt and Zheng-Yi Chen, cochlear gene delivery).